Neurology Flashcards
Define Essential Tremor
autosomal dominant condition affecting both upper limbs
features of essential tremor
postural tremor : worse if arms outstretch
improved by alcohol and rest
mc cause of titubation (head tremor)
management of essential tremor
propanolol - beta blocker - 1st line
sometimes used primidone
what is narcolepsy?
neurological disorder associated with excessive daytime sleeping
associated with HLA-DR2
associated with low levels of orexin (hypocretin) - this protein is responsible for controlling appetite and sleep patterns.
early onset of REM sleep
features of narcolepsy
typical onset: teenagers
hypersomnolence
cataplexy - sudden loss of muscle tone often triggered by emotion
sleep paralysis
vivid hallucinations on going to sleep or waking up
how would you investigate narcolepsy
multiple sleep latency EEG
Management of narcolepsy
daytime stimulants - eg MODAFINIL
nightime : sodium oxybate
what is normal pressure hydrocephalus?
reversible cause of dementia in elderly.
secondary to reduced CSF absorption at the arachnoid villi.
could be secondary to head injury, subarachnoid haemorrhage or meningitis.
classic triad of symptoms seen in normal pressure hydrocephalus?
urinary incontinence
dementia and bradyphrenia (slow in thinking and processing info)
gait abnormality - similar to PD
60% of pts will have all 3 at time of diagnosis.
sx typically develop over a few months.
imaging for normal pressure hydrocephalus
hydrocephalus with venticulomegaly in the abscence of or out of proportion to, sulcal enlargement
how would you manage normal pressure hydrocephalus?
ventriculoperitoneal shunting
10% pts that have shunts get significant comps like seizures, infection and intracerebral haemorrhages
What is a TIA?
transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia, without acute infarction.
usually lasting less than 24 hrs signs.
causes of tia
vascular cause - transient decrease in blood flow to the brain
clinical features of tia
sudden onset, focal neurological deficit - typically resolve within an hr
unilateral weakness or sensory loss
aphasia or dysarthria (difficulty forming/pronouncing words)
ataxia, vertigo, loss of balance
visual problems:
- diplopia
- homonymous hemianopia
- sudden transient loss of vision in 1 eye (amaurosis fugax)
what to do with patient that has acute focal neurological symptoms that resolve completely within 24 hrs of onset
aspirin 300mg immediately unless CI’d
assess within 24 hrs by stroke specialist
give 2 examples of TIA mimics
hypoglycaemia
intracranial haemorrhage : all pts on anticoagulants or with similar rf should be admitted for urgent imagine to exclude haemorrhage
what to do if a pt presents more than 7 days ago with tia?
see stroke specialist asap within 7 days
imaging for tia
ct - only useful if clinical suspicion of haemorrhage bc pt is taking anticoagulants
MRI - including diffusion-weighted and blood-sensitive sequences- determines the territory of ischaemia, or to detect haemorrhage or alternative pathology.
do same day as stroke specialist seen
medication for tia?
pts within 24 hrs of tia or minor ischaemic stroke , with low bleeding risk : dapt regime -
clopidogrel 300mg initial then 75 mg od + aspirin 300mg initial then 75mg od for 21 days. then continue clopidogrel
ticagrelor + clopi = alternative
if cant have DAPT:
clopi 300mg loading + 75 mg od forever.
could you PPI
what other drugs can you give to help with tia?
if AF pt. : anticoagulated as soon as intracranial haemorrhage excluded.
high intensity statin - atorvastatin 20-80 mg daily - reduce non-hdl cholesterol by more than 40%
why is it necessary to do carotid imaging for TIA patient?
atherosclerosis in carotid artery could be emboli source.
if carotid intervention, do carotid imagine within 24 hrs of assessment. - CAROTID DUPLEX USS, CT ANGIOGRAPHY OR MR ANGIOGRAPHY
what is the surgery for tia and when would you do it?
carotid endarterectomy - if pt suffered stroke/tia in carotid territory and isnt severely disabled.
if stenosis over 50%.
some have cut off of 70%
perform asap within 7 days
What is MND and what are the types?
neurological condition.
unknown cause.
presents with UMN and LMN signs.
rare before 40.
types:
amyotrophic lateral sclerosis (ALS)
primary lateral sclerosis
progressive muscular atrophy
progressive bulbar palsy
tell me what signs you see in ALS
50% of mnd cases
LMN signs in arms and UMN in legs
tell me what signs you see in primary lateral sclerosis (mnd)
umn signs only
tell me what signs you see in progressive muscular atrophy (MND)
LMN signs only
affects distal muscles before proximal
carries best prognosis
tell me the signs you see in progressive bulbar palsy (MND)
palsy of tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
WORST PROGNOSIS
features of ALS specific MND
assymetric limb weakness
mixed lmn and umn
features of mnd
wasting of small hand muscles/tibialis anterior common
fasciculations
absense of sensory signs/symptoms - vague sensory sx early in disease like limb pain- never sensory signs
doesnt affect external ocular muscles- eye movement
no cerebellar signs
abdominal reflexes preserved
sphincter dysfunction present (LATE FEATURE)
how to diagnose MND?
clinical
nerve conduction studies = normal motor conduction.
electromyography - reduced number of action potentials with increased amplitude.
MRI - exclude differentials : cervical cord compression and myelopathy.
how to manage MND?
Riluxole : prevents glutamate receptor stimulation. used in ALS. - prolongs life by 3 months
Resp: BIPAP - non invasive ventilation - @ night : survival benefit of 7 months
nutrition: PEG - percutaneous gastrostomy tube
prognosis: 50% pts die within 3 yrs
what is multiple sclerosis?
chronic cell-mediated autoimmune disorder characterised in CNS.
3* more common i women.
20-40 yrs old
higher latitudes more common
genetics associated with multiple sclerosis
monozygotic twin concordance = 30%
dizygotic twin concordance = 2%
subtypes of multiple sclerosis
relapsing remitting - 85% pts - acute attacks 1-2mths - followed with remission periods
secondary progressive : relapsing remitting deteriorated pts - neurological signs and sx between relpase.
65% of RR pts develop this within 15 yrs of diagnosis
gait and bladder disorders too
primary progressive : 10% pts - progressive deterioration from start. older people
features of multiple sclerosis
visual : optic neuritis, optic atrophy, internuclear opthalmoplegia, UHTOFF PHENOMENON: worsening of vision with rise in body temp.
sensory : pins/needles , numbness, trigeminal neuralgia, LHERMITTES SYNDROME: sharp pain/electric shock down spine (parasthesiae) in limbs on neck flexion forward.
motor: spastic weakness - in legs
cerebellar: ataxia (acute relapse not presenting sx) , tremor
others: urinary incontinence, sexual dysfunction intellectual deterioration
non specific: LETHARGY
criteria for diagnosing multiple sclerosis
2 or more relapses and
either
clinical evidence of 2 or more lesions
or
objective clinical evidence of 1 lesion together with reasonable historical evidence of previous relapse.
LESIONS DISSEMINATED IN TIME AND SPACE
investigations of multiple sclerosis
diagnosis requires demonstration of lesions DISSEMINATED IN TIME AND SPACE
MRI:
high signal T2 lesions.
periventricular plaques.
DAWSON FINGERS: FLAIR images : hyperintense lesions perpendicular to corpus callosum
CSF:
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG
Visual Evoked Potentials:
- delayed but well preserved waveform
How would you manage an acute relapse of multiple sclerosis?
high dose steroids - eg oral/iv methylpredinosolone
5 days TO SHORTERN LENGTH OF ACUTE RELAPSE.
dont alter degree of recovery. (whether pt return to baseline function)
what are the indications for disease modifying drugs for multiple sclerosis?
relapsing remitting disease + 2 relapses in past 2 yrs + able to walk 100m unaided
secondary progressive disease + 2 relapses in past 2 yrs + able to walk 10m (aided/unaided)
what are the different drug options for reducing relapse risk in MS.
how would you administer each?
natalizumab - strongest evidence base for reducing relapse - iv
ocrelizumab - iv
fingolimod - oral formulation
beta-interferon - subcut/intramuscularly
glatiramer acetate - subcut
tell me a little bit about natalizumab (MS tx drug)
recombinant monoclonal antibody that antagonises alpha 4 -beta-1 integrin found on surface of leucocytes
inhibit migration of leucocytes across endothelium across blood brain barrier.
1st LINE
tell me a little bit about ocrelizumab (MS TX)
humanized anti-cd20 monoclonal antibody
like natalizumab - high efficacy
natalizumab and ocrelizumab both used 1st line.
tell me a little bit about fingolimod (MS TX)
spingosine 1-phosphate (S1P) receptor modulator
prevents lymphocytes leaving lymph nodes
tell me a little bit about beta-interferon (MS TX)
not as effective as alternatvie disease modifying drugs like natalizumab and ocrelizumab
tell me a little bit about glatiramer acetate (MS TX)
immunomodulating drug - acts as immune decoy.
older drug - less effective than 1st line drugs
how would you treat fatigue in MS patients?
AMANTADINE
exclude anaemia, thyroid and depression first though.
other options: mindfulness training, CBT
how would you treat spasticity in MS patient?
baclofen and gabapentin : 1st LINE
other options:
diazepam, dantrolene and tizanidine
physio is important
cannabis and Botox - under evaluation
how would bladder dysfunction in MS pts?
could be urgency incontinence or overflow
GET USS to assess bladder emptying - anticholinergics could worsen sx in some pts
if signifcant residual volume - intermittent self catherisation
if no significant residual volume - anticholinergics - may improve urinary frequency
how would you treat oscillopsia (visual fields oscillate) in MS pts?
GABAPENTIN - 1ST LINE
features of duchenne muscular dystrophy
progressive proximal muscle weakness from 5 years
calf pseudohypertrophy (fat/connective tissue replacing muscle tissue so weak)
GOWERS sign: child uses arms to stand up from squatted position
30% of pts - intellectual impairement
how to investigate duchenne muscular dystrophy?
raised creatinine kinase
genetic testing replaced muscle biopsy for definitive diagnosis
how to manage duchenne muscular dystrophy?
largely supportive
no effective tx
prognosis of duchenne muscular dystrophy?
most children cant walk by 12 yrs old
patients typically survive to approx 25-30
associated with dilated cardiomyopathy
most common heart lesion associated with duchenne muscular dystrophy
dilated cardiomyopathy
tell me a little about becker muscular dystrophy?
develops after 10 yrs old
intellectual impairment much less common
talk to me about the genetics behind dystrophinopathies (duchenne and becker)
X LINKED
MUTATION IN GENE ENCODING DYSTROPHIN, dystrophin GENE ON Xp21.
what is dystrophin?
part of large membrane associated protein in muscle.
connects muscle membrane to actin. - part of muscle cytoskeleton.
genetic mutation in duchenne muscular dystrophy vs becker muscular dystrophy?
duchenne: frameshift mutation resulting in 1 or both of binding sites lost leading to severe form
becker: non-frameshift insertion in dystrophin gene - both binding sites preserved = milder form.
what is myotonic dystrophy?
inherited myopathy.
features develop at 20-30 yrs old.
affects skeletal, cardiac and smooth muscle.
2 types: DM1 AND DM2.
genetics of myotonic dystrophy
autosomal dominant
trinucleotide repeat disorder
DM1 : CTG repeat and the end of DMPK (dystrophia myotonica-protein kinase) gene on chromosome 19
DM2: repeat expansion of ZNF9 gene on chromosome 3.
key differences between DM1 AND DM2 - myotonic dystrophy?
dm1: DMPK gene on chr 19. DISTAL WEAKNESS more prominent
dm2: ZNF9 gene on chr3. Proximal weakness more prominent. severe congenital form not seen.
general features of myotonic dystrophy
myotonic facies, long, haggard appearance. atrophy of facial muscles and narrow face.
frontal balding
bilateral ptosis - eye lids drop down.
cataracts
dysarthria
myotonia (tonic spasm of muscle)
weakness of arms and legs - distal initially
mild mental impairement
DM
testicular atrophy
cardiac involvement: heart block, cardiomyopathy
dysphagia
What is huntingtons disease??
neurodegenerative condition inherited.
progressive. incurable.
results in death 20 yrs after initial symptoms develop.
genetics of huntingtons disease
autosomal dominant
trinucleotide repeat disorder : repeat expansion of CAG - phenomenon of anticipation seen - disease presents earlier age in successive generations
results in degeneration of cholinergic and gabaergic neurons in the striatum of the basal ganglia
due to defect in huntingtin gene on chromosome 4
features of huntingtons disease
typically after 35
chorea
personality changes - irritability, apathy, depression , intellectual impairement
dystonia
saccadic eye movement - quick shifts of both eyes that change point of fixation
how would you manage huntingtons disease
no tx.
supportive:
genetic counselling
physio - mobility improve , joint function and prevent contractures
SALT speech language therapy
tetrabenazine - chorea
antidepressant - ssri - depression
what is a brain abscess?
pus filled swelling in brain .
causes of brain abscess
extension of sepsis from middle ear or sinuses.
trauma
surgery to scalp
penetrating head injuries
embolic events from endocarditis.
presenting symptoms of brain abscess
depend on site of abscess - if motor cortex will present earlier.
headache - dull, persistent
fever - possibly absent - usually not swinging pyrexia (large temp fluctuations) seen with abscesses at other sites.
focal neurology - oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure
raised intracranial pressure:
nausea
papilloedema
seizures
if a patient has headache fever and focal neurology what should i think?
brain abscess
if someone says oculumotor nerve palsy what should i think?
drooping of eyelid - ptosis.
difficulty moving eye in certain directions
if someone says abducens nerve palsy what should i think?
difficulty moving affected eye laterally - inward deviation - esotropia
double vision.
investigations for brain abscess
imaging with CT scan
how would you manage brain abscess
surgery - craniotomy - abscess cavity debrided
abscess might reform because head is closed following abscess drainage
iv abx: iv 3rd gen cephalosporin + metronidazole
intracranial pressure mx : dexamethasone
meningitis organisms in children
neonatal to 3 months:
group B streptococcus : usually acquired from mother at birth. more common in low birth weight babies and following prolonged rupture of membranes. breaking of the amniotic sac more than 18-24 hours before delivery
1month to 6 yrs -
neisseria meningitidis - meningococcus
streptococcus pneumoniae - pneumococcus
haemophilus influenzae
greater than 6 years:
neisseria menigitidis - meningococcus
streptococcus pneumoniae - pneumococcus
tell me a little bit about meningitis vaccine
children always immunised against serotype A,C.
so B became mc cause of bacterial meningitis in UK.
BEXSERO released. - added to nhs immunisation
2 months
4 months
12-13 months.
also available to pts @ high risk of meningococcal disease like ppl with asplenia, splenic dysfunction or complement disorder.
symptoms of meningitis
headache
fever
n+v
photophobia
drowsiness
seizures
signs of meningitis
neck stiffness
purpuric rash - particularly with invasive meningococcal disease
csf findings for bacterial meningitis
appearance
glucose
protein
white cells
cloudy appearance
glucose : Low - <1/2plasma
Protein: high >1g/L
White cells: 10-5000 polymorphs/mm3
csf findings for viral meningitis
appearance
glucose
protein
white cells
clear/cloudy appearance
glucose: 60-80% of plasma glucose
protein: normal/raised
white cells: 15-1000 lymphocytes/mm3
csf findings in tuberculous meningitis
appearance
glucose
protein
white cells
slight cloudy, fibrin web
glucose: low <1/2 plasma
protein : high >1 g/L
white cells: 10-1000 lymphocytes/mm3
for detection of tuberculous meningitis what is used?
PCR - sensitivity 75%
ziehl-neelsen stain only 20% sensitive.
for viral meningitis, what are the exceptions to the rule for csf findings of glucose?
mumps and herpes encephalitis - has low glucose level in some cases.
why might it be hard to diagnose meningitis clinically?
classical signs are often absent in infants in bacterial meningitis
sx can progress rapidly and often become more specific and severe with time.
causative agents of meningitis
0-3 months:
group B streptococcus - mc in neonates
e.coli
listeria monocytogenes
3mnths- 6yrs:
neisseria meningitidis
streptococcus pneumonia
haemophilus influenzae
6yrs - 60 yrs:
neisseria meningitidis
streptococcus pneumonia
> 60yrs:
streptococcus pneumoniae
Neisseria meningitidis
listeria monocytogenes
immunosuppressed:
listeria monocytogenes
complications of meningitis
seizures
focal neurological deficit
infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus
sensorineural hearing loss (MC) - inner ear/auditory nerve damage = difficulty hearing faint sounds and understanding speech.
what are patients with meningococcal meningitis at risk of
waterhouse - friderichsen syndrome - adrenal insufficiency secondary to adrenal haemorrhage
what would be some contraindications to carrying out a lumbar puncture for meningitis?
any signs of raised ICP
focal neurological signs - impairments in the function of the brain, spinal cord, or nerves that affect a specific area of the body
papilloedema - SWELLING OF OPTIC DISK DUE TO INCREASE ICP
significant bulging of fontanelle
disseminated intravascular coagulation
signs of cerebral herniation
PATIENTS WITH MENINGOCOCAL SEPTICAEMIA - DO BLOOD CULTURES AND PCR INSTEAD.
how to manage meningitis
- abx - if under 3months: iv amoxicilllin (or ampiciliin) + iv cefotaxime
if over 3 months: iv cefotaxime (or ceftriaxone) - steroids - NOT FOR CHILDREN UNDER 3 MONTHS.
dexamethasone if lumbar puncture shows:
- frankly purulent csf
-csf wbc over 1000/microleter
- raised csf wbc with protein conc over 1g/L
- bacteria on gram stain - fluids - treat any shock eg with colloid
- cerebral monitoring - mechanical ventilation if resp impairement
- public health - notify and abx prophylaxis of contacts.
GIVE CIPROFLOXACIN OVER RIFAMPICIN.
WHAT IS MENINGITIS
INFLAMMATION OF LEPTOMENINGES AND CSF IN SUBARACHNOID SPACE.
what is viral meningitis
inflammation by viral agent in leptomeninges
causes of viral meningitis
non-polio enteroviruses eg - coxsackie virus, echovirus
mumps
herpes simplex virus - HSV, cytomegalovirus (CMV), herpes zoster viruses
HIV
MEASLES
risk factors of viral meningitis
patients at extremes of age - under 5 and elderly
immunocompromised - eg patients with renal failure with diabetes
iv drug users.
clinical presentation of viral meningitis
headache
neck stiffness
photophobia - often milder than that of bacterial meningitis
confusion
fever
less common:
focal neurological deficit on exam
seizures: suggests meningoencephalitis
investigations for viral meningitis
csf :
opening pressure - 10-20cm3 h20
cell count - 10-300 cells/uL
cell diff: lymphocytes
glucose : 2.8-4.2 mmol/l or 2/3 serum glucose mmol/L
protein : 0.5-1 g/dL (0.15-0.45 g/L)
viral pcr - underlying organism
how to manage viral meningitis
whilst waiting on lumbar puncture: supportive . if you think bacterial/encephalitis then start broad spec abx with cns penetration : CEFTRIAXONE AND ACICLOVIR IV. particularly in elderly, immunocompromised
viral meningitis self limiting, sx improving over the course of 7-14 days. comps are rare in immunocompetent patients.
what to use if the patient is suspected of having meningitis secondary to HSV?
Aciclovir
managing suspected bacterial meningitis?
initial approach in hospital
if patient in gp : give IM benzylpenicillin as long as it dont delay hospital transit.
ABC - initially
airway
breathing
circulation
disability : gcs, focal neurological signs: seizures, papilloedema
senior review if warning signs are present
give some warning signs of meningitis as per investigation/mx of it (bacterial)
rapidly progressive rash
poor peripheral perfusion
rr : less than 8 or over 30/min or pulse rate under 40 or over 140/min
ph less than 7.3
wbc less than 4*10 power of 9/L or lactate over 4 mmol/L
gcs under 12 or drop of 2 pts
poor response to fluid resus.
in what circumstances should a lumbar puncture be delayed?
signs of severe sepsis or rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised icp:
focal neurological signs
papilloedema
continuous/uncontrolled seizures
GCS 12 OR MORE.
how would you manage bacterial meningitis patients without indication for delayed LP?
iv access = take bloods and blood cultures
NO NEED FOR CT
lumbar puncture : if you cant in 1st hr, iv abx after blood cultures
iv abx: 3mnths-50yrs : cefotaxime (or ceftriaxone)
over 50: cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin) for adults.
iv dexamethasone (consider adjuncting with it if pneumoccocal meningitis). start before or with 1st dose of antibacterial. not later than 12 hrs after.
in what case would you avoid iv dexamethasone in bacterial meningitis pt ?
septic shock
meningococcal septiciaemia
immunocompromised
meningitis following surgery
how would you manage patients with bacterial meningitis that have signs of raised intracranial pressure?
critical care input
secure airway + high flow oxygen
iv acess= take blood + blood cultures
iv dexamethasone
iv abx cefotaxime or ceftriaxone
arrange neuroimagine
how would you manage bacterial meningitis patients that have signs of severe sepsis or rapidly evolving rash?
critical care input
secure airway + high flow o2
iv access = bloods+ blood culture
iv fluid resus
iv abx
when you take bloods for bacterial meningitis pt, what should they include?
fbc
renal function
glucose
lactate
clotting profile
crp
if an LP is done for suspected bacterial meningitis , what should the csf be tested for?
glucose protein microscopy and culture
lactate
meningococcal and pneumococcal PCR
enteroviral, herpes simples and varicella zoster PCR
consider ix for tb meningitis
other than blood and an LP what tests could be useful in a bacterial meningitis suspected pt?
blood gases
throat swab for meningococcal culture
pt has been found to have bacterial meningitis : pneumoccal meningitis. what is the treatment?
iv cefotaxime (of ceftriaxone)
pt has been found to have bacterial meningitis, specifically meningococcal meningitis. how would you treat?
iv benzylpenicillin or cefotaxime (or ceftriaxone)
pt has been found to have bacterial meningitis specifically meningitis caused by haemophilus influenze. how to treat?
iv cefotaxime (of ceftriaxone)
patient has bacterial meningitis, caused by listeria. how to treat?
iv amoxicillin (or ampicillin) + gentamicin
who should prophylaxis of meningitis (bacterial) be offered to?
how long does risk last for?
households and close contacts of pts with meningococcal meningitis.
exposed to resp secretion , regardless of closeness.
risk is highest in 1st 7 days but stays for 4 weeks.
what is the prophylactic tx for close contacts?
give within 7 days before onset.
oral ciprofloxacin or rifampicin.
cipro only requires 1 dose.
meningoccocal vaccination offered to close contacts when serotype results are available including booster doses.
pneumoccocal meningitis: no prophylaxis needed. only if cluster of cases give abx.
what is guillain-barre syndrome?
immune mediated demyelination of peripheral nervous system often triggered by infection
CAMPLYOBACTER JEJUNI
what is the pathogenesis of guillain-barre syndrome?
cross reaction of antibodies with gangliosides in the peripheral nervous system.
correlation between anti-ganglioside antibody (anti-GM1) and clinical features has been demonstrated.
anti- GM1 antibodies in 25% of pts.
what is miller fisher syndrome?
variant of guillain-barre syndrome
associated with:
opthalmoplegia
areflexia
ataxia.
eye muscles typically affected first.
presents with descending paralysis rather than ascening.
anti- GQ1B antibodies in 90% of cases.
what initial symptoms will you notice with guillain- barre syndrome?
65% pts experience back/leg pain in initual stages
characteristic features of gullain-barre syndrome
progressive symmetrical weakness of all the limbs.
ASCENDING. - legs affected first.
reflexes reduced/absent
sensory symptoms tend to be mild (distal paresthesia) - very few sensory signs
general other features of guillain- barre syndrome
history of gastroenteritis
respiratory muscle weakness
cranial nerve involvement: diplopia, bilateral facial nerve palsy, oropharyngeal weakness common
autonomic involvement: urinary retention, diarrhoea
less common: papilloedema: secondary to reduced csf resorption
what investigations would you do for guillain-barre syndrome?
lumbar puncture- rise in protein with normal wbc (ALBUMINOCYTOLOGIC DISSOCIATION) - found in 66%
nerve conduction studies -
decreased motor nerve conduction velocity - due to demyelination
prolonged distal motor latency
increased F wave latency
how would you manage guillain barre syndrome?
supportive
vte prophylaxis - pe leading cause of death
iv immunoglobulines - IVIG - 1st line
plasmapharesis - alternative to 1st line
severe cases might have resp failure: intubate, ventilate, admit to icu.
prognosis of guillain-barre
months to years.
continue regaining function 5 yrs after acute illness.
most get full recovery or have minor sx.
some have significant disability.
mortality 5% - due to resp or cardio complications
features of encephalitis
fever headache psychiatric symptoms, seizures vomiting
focal features: aphasia (language disorder)
peripheral lesions (cold sores) - have no relation to Prescence of HSV encephalitis
pathophysiology of encephalitis
hsv-1 responsible for 95% of cases in adults
typically affects temporal and inferior frontal lobes
how would you investigate encephalitis?
csf: lymphocytosis, elevated protein,
PCR FOR HSV,VSV AND ENTEROVIRUSES.
neuroimaging:
- medial temporal and inferior frontal changes (eg petechial haemorrhages)
- normal in 1/3 of pts
- MRI is better
EEG:
- lateralised periodic discharges at 2 Hz
how would you manage encephalitis
IV Aciclovir - started in all cases of suspected encephalitis
ct head shows temporal lobe changes, and pt has temporal lobe signs like aphasia. what should i think
herpes simplex encephalitis
prognosis of encephalitis
depends on if aciclovir is commenced early.
if started promptly, mortality 10-20%.
untreated it goes to 80%.
what is shingles?
herpes zoster infection.
acute unilateral painful blistering rash caused by reactivation of varicella-zoster virus (vzv).
after primary infection - chicken pox (VZV) - the virus lies dormant in the dorsal root or cranial nerve ganglia.
risk factors of shingles
increasing age
HIV - strong risk factor.
15 times more common
other immunosuppressive conditions (eg steroids, chemo)
most commonly affected dermatomes for shingles
T1-L2
features of shingles
prodromal period:
- burning pain over affected dermatome for 2/3 days
- pain might be severe and sleep interference.
- 20% pts experience fever, headache, lethargy
rash:
- initially erythematous , macular rash over affected dermatome
- quickly becomes vesicular
- well demarcated by dermatome. doesnt cross midline. some “bleeding” into adjacent areas might be seen.
diagnosis of shingles
clinical
management of shingles
tell pts its infectious! - avoid pregnant and immunosuppressed. infectious until vesicles cruster over, 5-7 after onset
analgesia:
para and nsaids = 1st line
if not then : neuropathic agent : amitriptyline
oral corticosteroids - consider in 1st 2 weeks in immunocompetent adults with localised shingles if pain is severe and not responding to above.
antivirals - GIVE WITHIN 72 HOURS unless if pt. is under 50 and has “mild” truncal rash associated with mild pain and no underlying risk factors.
examples:
aciclovir, famciclovir, valaciclovir
give a benefit of prescribing antivirals for shingles pt
reduced incidence of post-herpetic neuralgia - particularly in older people
complications for shingles
post-herpetic neuralgia:
- most common complications
- more common in older pts
- affects between 5-30% of pts depending on age.
- most commonly resolves with 6 months but may last longer
herpes zoster ophthalmicus - (shingles affecting affecting the ocular division of trigeminal nerve)
herpes zoster oticus (Ramsay hunt syndrome)- may results in ear lesions and facial paralysis
define malaria
a disease caused by plasmodium protozoa which is spread by the female anopheles mosquito.
4 different species that cause malaria
plasmodium falciparum
plasmodium vivax
plasmodium ovale
plasmodium malariae
which plasmodium for malaria causes most severe malaria?
plasmodium falciparum.
after that vivax is most common, causes “benign” malaria
protective factors for malaria
sickle-cell trait.
g6pd deficiency
hla-b53
absense of duffy antigens (proteins on surface of rbc involved in entry of malaria vivax into cells)
clinical features of the most common and severe type of malaria : falciparum
sx like flu. (malaise, headache and myalgia)
classic triad: paroxysms of fever, chills and sweating.
sx occur every 48 hrs. - correspond to erythrocytic cycle of plasmodium falciparum parasite.
fever high and intermittent. - poss rigors too.
general features of falciparum malaria
fever: cyclical. poss sweating and rigors
gi: anorexia, n+v + abdo pain. diarrhoea (sometimes in kids), poss mild jaundice and pruritus
resp: cough, poss mild tachypnoea.
msk: general body aches and joint pain
neuro: headache prominent and severe. dizziness and sleep disturbance.
cv: tachycardia poss, hypotension typical of more severe malaria.
haem: thrombocytopenia, can happen in absence of severe disease. mild anaemia poss
renal: aki associated with severe malaria. non severe could have mild to moderate increases in creatinine or blood urea nitrogen levels.
features of severe falciparum malaria
schizonts on a blood film
parasitaemia over 2%
hypoglycaemia
acidosis
temperature over 39
severe anaemia
complications (another card)
complications of falciparum malaria
cerebral malaria: seizures, coma
acute renal failure: blackwater fever, secondary to intravascular haemolysis
acute resp distress syndrome (ARDS)
hypoglycaemia
disseminated intravascular coagulation (DIC)
how would you manage uncomplicated falciparum malaria
strains resistant to chloroquine are prevalent in some parts of asia and africa
artemisinin-based combination therapy: 1st line
eg: arthemer + lumefantrine.
artesunate + amodiaquine
artesunate + mefloquine
artesunate + sulfadoxine- pyrimethamine
dihydroartemisinin + piperaquine
how would you treat severe falciparum malaria?
if parasite count over 2% then parenteral tx regardless of clinical state.
iv artesunate better than iv quinine
if parasite count over 10% - exchange transfusion consider
shock might indicate coexistent bacterial septicaemia = malaria rarely causes haemodynamic collapse
most common nonfalciparum malaria
vivax
then ovale and malariae
where is non falciparum vivax found
ovale?
knowlesi?
central america
indian subcontinent
ovale from africa
knowlesi - causes clinical pathology - south east asia
features of non falciparum malaria
fever headache splenomegaly
vivax/ovale: cyclical fever every 48 hrs
malariae: cyclical fever every 72 hrs. nephrotic syndrome association
why might ovale and vivax malaria relapse after treatment
they have a hypnozoite stage
treatment of non falciparum malaria
if chloroquine sensitive then artemisinin based combo therapy or chloroquine
if chloroquine resistant then defo ACT. avoid in pregnancy
if ovale/vivax: primaquine after acute tx with chloroquine to destroy liver hypnozoites and prevent relapse.
what is acoustic neuroma? (vesitbular schwannoma)
accounts for 5% of intracranial tumours and 90% of cerebellopontine angle tumours.
classic history of acoustic neuroma
combo of vertigo, hearing loss, tinnitus with absent corneal reflex.
features of acoustic neuroma can be predicted by the affected cranial nerves. tell me about this.
cranial nerve 8,5,7
CN VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
CN V : absent corneal reflex
CN VII: facial palsy
in what condition would you see bilateral vestibular schannomas (acoustic neuromas)
neurofibromatosis type 2
what to do if suspected vestibular schwannoma (acoustic neuroma)?
include investigations
refer urgent to ENT. some tumours are slow, benign and often observed initially.
MRI of cerebellopontine angle.
audiometry - only 5% pts will have normal audiogram.
management of acoustic neuroma (vestibular schwannoma)
surgery
radiotherapy
or observation
what is a subdural haemorrhage?
colleciton of blood deep to the dural layer of meninges.
its not within the substance of the brain so its called “extra-axial” or “extrinsic” lesion.
can be uni/bi lateral.
how can you classify subdural haematoma:
acute
sub acute
chronic
in terms of its age
acute: sx develop within 48 hrs of injury - rapid neurological deterioration
subacute: sx manifest within days to weeks post-injiury - gradual progression
chronic: common in elderly - weeks to months. - pts might not remember specific head injury
typical presentation of subdural haematoma
hx of head trauma minor-severe.
lucid interval - temp recovery of gcs after initial loss. - then gradual decline in conciousness. (very common in chronic sdh)
headache
confusion
lethargy
neurological symptoms of subdural haemorhage
altered mental status: mild confusion - deep coma. fluctuations in level of gcs common.
focal neurological deficit: weakness on 1 side of body, aphasia (ability to speak), visual field defects, depending on haematoma location.
headache : often localised to 1 side, worsening over time.
seizures: possible, more chance in acute/expanding haematoma.
what physical examination findings would you find in subdural haematoma patient?
papilloedema: shows raised ICP
pupil changes: unilateral dilated pupil (side of haematoma)- shows compression of 3rd cranial nerve
gait abnormalities: including ataxia or weakness in 1 leg.
hemiparesis(partial paralysis 1 side of body)/hemiplegia (full paralysis 1 side of body): reflecting mass effect and midline shift
what behavioural and cognitive changes would you see in subdural haemorrhage patient?
memory loss : esp in chronic SDH
personality changes: irritability, apathy, depression
cognitive impairment: attention difficulty, problem-solving, other executive functions
general features of subdural haemorrhage
n+v : secondary to raised ICP
drowsiness: progressing to supor and coma in severe cases.
signs of icp : bradycardia, hypertension, respiratory irregularities (cushings triad)
tell me about an acute subdural haematoma
collection of blood in subdural space. high impact trauma. possible underlying brain injuries too.
spectrum of sx and presentation depends on size of compressive acute subdural haematoma.
ranges from incidental finding in trauma to severe coma and coning due to herniation.
what investigation to do for acute subdural haematoma? and findings?
CT : 1st line
crescentic collection not limited by suture lines.
hyperdense (bright) compared to brain, .
large acute subdural haematoma will push on the brain (mass effect) and cause midline shift/herniation.
how to manage acute subdural haematoma?
small/incidental acute subdural: conservatively observe.
surgery: monitor of ICP and decompressive craniectomy
tell me a little bit about chronic subdural haematoma
collection of blood within subdural space present for weeks to months.
rupture of small bridging veins in subdural space - slow bleeding.
who is at risk of chronic subdural haematoma?
why?
elderly and alcoholic pts.
they have brain atrophy - so fragile or taut bridging veins.
infant: shaken baby syndrome. fragile bridging veins
presentation of chronic subdural haematoma
several week to month progressive hx of either confusion, reduced gcs or neurological deficit.
how would you investigate chronic subdural haemorrhage?
findings
CT - crescentic in shape not restricted by suture lines and compress the brain (mass effect)
different to acute bc:
hypodense (Dark) compared to substance of brain
management of chronic subdural haemorrhage
if incidental finding or small in size with no neurological deficit : conservative mx. hope itll dissolve with time.
if pt confused, has associated neurological deficit or has severe imagine findings: SURGICAL DECOMPRESSION WITH BURR HOLES. (burr hole evacuation)
what is a subarachnoid haemorhage?
intracranial haemorrhage.
blood within subarachnoid space - deep to subarachnoid layer of meninges.
causes of subarachnoid haemorrhage
most common : head injury (traumatic SAH)
if not trauma then spontaneous.
spontaneous:
- intracranial aneurysm (saccular “berry” aneurysm) - 85%.
- arteriovenous malformation
- pituitary apoplexy
- mycotic (infective) aneurysm
conditions associated with berry aneurysms (subarachnoid haemorrhage)
htn
adult polycystic kidney disease (ADPKD)
ehlers-danlos syndrome
coarctation of aorta
classic presenting features of subarachnoid haemorrhage
headache - sudden onset, thunderclap, severe(worst of life), occipital, typically peaks in intensity within 1-5 mins.
could be hx of less-severe sentinel headahce weaks prior.
n+v
meningism - photophobia, neck stiffness
coma
seizures
ecg changes: st elevation. secondary to autonomic neural stimulation from hypothalamus/elevated levels of circulating catecholamines.
investigations of subarachnoid haemorrhage
non-contrast CT head : 1st line. - acute blood hyperdense bright. - distributed in basal cisterns, sulci and in severe case ventricular system.
if ct head done within 6hrs and normal - no LP. consider alternative diagnosis
if ct head done more than 6 hrs after and is normal - do LP. LP at least 12 hrs after sx start to allow xanthochromia to develop. ( result of rbc breakdown)
if ct shows evidence of SAH: refer to neurosurgery.
what does xanthochromia help to distinguish in LP for SAH patient?
traumatic tap (blood introduced by LP procedure)
what csf findings are consistent with SAH?
xanthochromia
normal or raised opening pressure
what investigations to do once spontaneous SAH is confirmed?
why?
identify causative pathology that needs urgent tx
CT intracranial angiogram - identify vascular lesion (aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)
how would you manage a confirmed aneurysmal subarachnoid haemorrhage?
supportive: bed rest, analgesia, VTE prophylaxis, discontinue antithrombotics (reversal of anticoagulation if present)
oral nimodipine: prevent vasospasm
COIL: intracranial aneursym - bc of risk of bleeding. small minority need craniotomy and clipping. - WITHIN 24 HRS
complications of aneurysmal SAH
seizures
re-bleeding - 10% in 1st 12hrs. if suspected so sudden worsened sx then repeat CT. high morality 70%
hydrocephalus - temp tx with external ventricular drain (csf diverted into bag at bedside) - long term : ventriculoperitoneal shunt)
vasospasm: (delayed cerebral ischaemia) - typically 7-14 days after onset.
hyponatremia - typically due to SIADH
what would you do to treat vasospasm as comp of aneurysmal SAH?
ensure euvolemia - normal blood volume
consider tx with vasopressor if sx persist.
name 3 important predictive factors in SAH
age
amount of blood on CT head
conscious level on admission
what is an extradural haematoma?
where is the collection usually?
collection of blood between skull and dura.
almost always trauma - most typically low impact. (blow to head/fall).
collection: temporal region because the thin skull at pterion overlies the MIDDLE MENINGEAL ARTERY = vulnerable to injury.
classic presentation of patient with extradural haematoma
loses,gains,loses gcs after low impact injury. (brief regain is called lucid interval)
you lose it again due to expanding haematoma and brain herniation.
treatment of extradural haematoma
if no neurological deficit: cautious clinical and radiological obs appropriate.
definitive: craniotomy and evacuation of haematoma
imaging of extradural haematoma
ct
biconvex (or lentiform) hyperdense collection around surface of brain.
limited by suture lines of the skull.
explain why you lose the lucid interval in patient with extradural haemorrhage/haematoma?
expanding haematoma and brain herniation.
As haematoma expands the uncus of temporal lobe herniates around tentorium cerebelli
pt develops fixed and dilated pupil due to compression of parasympathetic fibers of 3rd cranial nerve.
what is a febrile convulsion?
seizure provoked by fever in otherwise normal kids.
6months - 5 years
3% of kids
clinical features of febrile convulsions
usually occur early in viral infection as temp rises rapidly
brief, lasting less than 5 mins
most commonly tonic-clonic
types of febrile convulsions
simple : under 15 mins. generalised seizure. typically no recurrence within 24 hrs. should be complete recovery within nan hr.
complex: 15-30 mins. focal seizure. might have repeat seizures within 24hrs
febrile status epilepticus : over 30 mins
how would you manage a febrile convulsion seizure?
if 1st seizure / complex seizure - admit to paeds
parents phone ambulance is seizure over 5 mins
regular antipyretics dont reduce change of febrile convulsion happening
if recurrent febrile convulsion then benzodiazepine rescue med. - RECTAL DIAZEPAM/BUCCAL MIDAZOLAM
risk of further febrile convulsion.
what does it depend on?
1/3
age of onset under 18months
fever under 39
shorter duration of fever before seizure
fhx of febrile convulsion
can you tell me a little bit about the link between epilepsy and febrile convulsions?
fhx of epilepsy, complex febrile seizures and background of neurodevelopmental disorder
what is trigeminal neuralgia?
causes
pain syndrome characterised by severe unilateral pain.
idiopathic
could get compression of trigeminal roots by tumours or vascular problems
presentation of trigeminal neuralgia
how is pain evoked
unilateral
brief electric shock pain
limited to 1 or more division of trigeminal nerve.
pain evoked by light touch : washing, shaving, smoking, talking, brushing teeth.
where is pain usually evoked in trigeminal neuralgia?
small areas in nasolabial fold or chin.
name some red flag symptoms that suggest serious underlying cause of trigeminal neuralgia?
sensory changes
fhx of MS
onset before 40
optic neuritis
deafness/other ear problems
hx of skin/oral lesions that could sprewad perineurally
pain only in opthalmic division of trigeminal nerve - eye socket,forehead,nose - or bilaterally
how would you manage trigeminal neuralgia?
carbamazepine - 1st line
if they dont respond or have atypical features - like under 50: refer to neuro
tell me about diabetic neuropathy
glove and stocking sensory loss.
no motor loss.
lower legs affected 1st due to length of sensory neurones supplying the area.
sometimes you see painful diabetic neuropathy
how would you manage neuropathic pain (diabetic neuropathy managed same way)
1st line: amitryptiline, duloxetine, gabapentin, pregabalin
if 1st line dont work, try one of others
tramadol - rescue therapy - for exacerbations of neuropathic pain.
topical capsaican :: localised neuroapthic pain - post-herpetic neuralgia
pain management clinic?
why does gastro-oeseophageal reflux disease happen?
decreased lower esophageal sphincter (les) pressure
what happens in GI autonomic neuropathy
gastroparesis - 2ndary to autonomic neuropathy. erratic bg , bloating + vomiting. mx: metoclopramide, domperidone or erythromycin (prokinetic agents)
chronic diarhoea - @ night
GORD
what is giant cell arteritis: temporal arteritis?
vasculitis of unknown cause - affecting medium + large sized vessels arteries.
over 50.
peak incidence: 70’s
features of temporal arteritis
typical patient over 60.
rapid onset (under month)
headache (found in 85%)
jaw claudication (65%)
anterior ischaemic optic neuropathy .
possible temporary vision loss - amaurosis fugax
permanent visual loss - feared comp of gca and could suddenly happen.
diplopia - results from involvement of any part of oculomotor system - eg cranial nerves
- tender , palpable temporal artery
- 50% pts have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
- also lethargy , depression, low-grade fever, anorexia, night sweats
in giant cell arteritis , why does anterior ischaemic optic neuropathy occur?
occlusion of posterior ciliary artery - branch of opthalmic artery.
ischaemia of optic nerve head.
fundoscopy shows swollen pale disc and blurred margins.
what investigations would you do for gca?
raised inflammatory markers:
- esr >50 mm/hr (esr under 30 in 10% pts)
crp could be elevated
temporal artery biopsy: skip lesions possibly present
creatine kinase and EMG normal
how to treat GCA?
urgent high-dose glucocorticoids asap when diagnosis suspected before temporal artery biopsy
if no visual loss: high dose prednisolone
if evolving visual loss - iv methylprednisolone prior to starting high-dose pred
should be dramatic response
urgent opthalmology review :
- pts with visual sx same day review bc visual damage often irreversible.
other tx:
bone protection - bisphosphonates as long as required - tapering course of steroids.
low dose aspirin - sometimes.
what is bells palsy?
acute
unilateral
idiopathic
facial nerve paralysis.
unknown aetiology.
peak incidence: 20-40.
more common: pregnant women
features of belly palsy
lower motor neuron facial nerve palsy - forehead affected. - in contrast to umn lesion spares the upper face.
patients also notice:
- altered taste
-dry eyes
-post-auricular pain (may precede paralysis)
- hyperacusis
how would you manage bells palsy?
oral prednisolone within 72 hours of onset.
debate about adding antiviral meds (esp if severe facial paralysis)
eye care important to prevent exposure keratopathy : artificial tears, eye lubricants. - if cant close eye at bedtime tape it with microporous tape
follow up for bells palsy
if paralysis no sign of improvement after 3 weeks, refer urgently to ENT
refer to plastics for pts with more long standing weakness- eg several months
prognosis of bells palsy
most ppl full recovery within 3-4 months
if untreatred, 15% pts permanent moderate to severe weakness
what is cerebral palsy?
disorder of movement and posture due to non-progressive lesion of motor pathways in developing brain.
2/1000 live births
MC cause of major motor impairement
causes of cerebral palsy
antenatal (80%) - cerebral malformation and congenital infection (rubella,toxoplasmosis, CMV)
intrapartum (10%) - birth asphyxia/trauma
postnatal (10%) - intraventricular haemorrhage, meningitis, head trauma
classifications of cerebral palsy
spastic - 70% - hemiplegia, diplegia, or quadriplegia
dyskinetic
ataxic
mixed
manifestations of cerebral palsy
abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulty
what non-motor problems do children with cerebral palsy have?
learning difficulty - 60%
epilepsy (30%)
squints (30%)
hearing impairment (20%)
how would you manage a pt with cerebral palsy
multidisciplinary approach - child - chronic
tx:
spasticity - oral diazepam , oral and intrathecal baclofen, botulinum toxin type A , orthopaedic surgery and selective dorsal rhizotomy
- anticonvulsants , analgesia as required
what is hypoxic-ischaemic encephalopathy?
serious neuro condition due to inadequate cerebral oxygen supply.
associated with perinatal asphyxia in neonates.
can occur in adults due to cardiac arrest or severe systemic hypoxia.
2 types : primary energy and secondary energy failure
tell me about primary energy failure - hypoxic ischaemic encephalopathy?
occurs immediately during HIE.
leading to anaerobic metabolism, lactic acidosis and cytotoxic oedema.
after initial resus and reoxygenation , a period of latent phase occurs where the brain appears to recover.
tell me about secondary energy failure - HIE
hours to days later occurs
renewed accumulation of toxic metabolites and free radicals causing further neuronal death.
clinically, HIE presents with
altered consciousness levels ranging from lethargy to coma, seizures, abnormal tone and reflexes
how would you manage HIE?
supportive care :
- maintaining normal body temp
blood glucose
seizure control.
therapeutic hypothermia : shown benefits in neonatal HIE if initiated within 6 hrs of birth.
1st line ix for HIE
ABG - extent of met acidosis, hypercapnia, hypoxemia.
complete blood count - underlying infection, anaemia, polycythaemia
serum electrolytes and glucose - sodium potassium calcium and glucose - detect imbalances that can exacerbate neuro injury
lft + renal function test: liver enzymes and renal function markers eg creatinine and urea.
what neuroimaging would you do for HIE
cranial ultrasound:
in neonates non-invasive 1st line. detects intracranial haemorrhage or structural abnormality.
sensitivity is limited in early HIE
MRI brain : diffusion weighted imaging - gold standard.
within 2-5 days post injury. assess brain injury.
look for patterns like :
watershed infarcts
basal ganglia/thalamic involvement
tell me some amplicative ix for HIE?
EEG : check subclinical seizures. brain activity.
continuous if suspect seizures or severe encephalopathy.
aEEG: amplitude - integrated eeg - continuous bedside monitoring in neonatal units. rapid assessment of cerebral function over time.
what to do if there are atypical features of HIE suggesting metabolic disorder?
do met screening
ammonia levels
lactate
pyruvate
plasma A.A
urine organic acids
tandem mass spectrometry for acylcarnitine profile analysis.
also do if:
- inborn error of metabolism based on clinical presentation/fhx.
- if mitochondrial disorders like elevated lactate-to-pyruvate ratio. specific neuroimaging findings like basal ganglia lesions.
name some complications of HIE
cerebral palsy - common outcome - often involving spastic quadriplegia or dyskinetic form.
poor growth - feeding difficulty - neurological impairement
microcephaly - reduced head circumference - due to impaired brain growth.
behavioural disorders: adhd, asd
sensory : visual , auditory deficit frequent. cortical visual impairment and sensorineural hearing loss.
congitive impairement: mild learning difficulty to severe intellectual disability.
seizure disorders: neonates develop symptomatic seizures intially and later epilepsy.
severe cases:
multisystem organ failure - cv,renal,hepatic,respiratory systems.
what is a migraine?
common headache.
severe unilateral throbbing
nausea
photophobia
phonophobia
attacks can last upto 72 hrs.
pts usually go into dark,quiet room during attack
what is an aura?
happens before headache. precipitates migraine.
1/3 of migraine pts.
visual progressive last 5-60 mins .
characterised by transient hemianopic disturbance or a spreading scintillating scotoma.(flashing lights)
epidemiology of migraine
3 times more in women
common triggers of migraine
tiredness, stress
alcohol
combined oral ccp
lack of food/dehydration
cheese,chocolate,red wines, citrus fruits
menstruation
bright lights
migraine diagnostic criteria
at least 5 attacks fulfilling b-d
b - lasts 4-72 hrs - untx or unsucessfully tx
c headache at least 2 of following:
- unilateral
- pulsating
-moderate/severe pain
- aggravation bby or causing avoidance of routine physical activity
d - during headache at least one of:
- nausea and/or vomiting
- photophobia and phonophobia
e - no other cause.
what is a hemiplegic migraine?
variant.
motor weakness manifestation of aura in some attacks.
half pts have strong fhx
very rare - 0.01%
more common in adolescent females
aura sx
fully reverisble, develop over 5 mins, last 5-60 mins
motor weakness
double vision
poor balance
decreased gcs
visual sx affecting only 1 eye
how to manage migraine
5-ht receptor agonist in acute tx
5-ht receptor antagonist -prophylaxis
acute
1st line : combination - oral triptan and nsaid , or
oral triptan + paracetamol
if 12-17 - nasal triptan
if not effective
non-oral prep of metoclopramide or prochlorperazine and can add non-oral nsaid or triptan.
what can develop when giving metoclopramide in young pts with migraine?
acute dystonic reaction
prophylaxis of migraine
propranolol
topiramate - avoid in women of child bearing age - teratogenic - reduces hormonal contraceptive effectiveness
amitriptyline
10 sessions of accupuncture over 5-8 weeks
riboflavin 400mg od - can reduce frequency and intensity for some.
for women with predictable menstrual cycle, how to prophylaxis for migraine?
frovatriptan 2.5 mg twice a day
zolmitriptan 2.5 mg twice or 3 times a day
miniprophylaxis
why isnt pizotifen no longer recommended for migraine prophylaxis?
weight gain
drowsiness
how to treat migraine during pregnancy?
paracetamol 1g : 1st line
nsaids second line in 1st and second trimester
avoid aspirin and opioids eg codeine
pt has migraine with aura, wants to take oral contraceptive, what to do ?
contraindicated due to increased risk of stroke
can i prescribe hormone replacement therapy for migraine pt?
safe but might make migraines worse
link between migraine and menstruation
lots pts say frequency and severity increase around menstruation
tx with mefanamic acid
or combo of
aspirin paracetamol and caffeine.
triptans also in acute situation
clinical features of tension headache
tight band around head or pressure sensation.
bilateral
lower intensity than migraine
no aura, n+v, or aggravated by physical activity.
could be stress related
could co-exist with migraine
what is a chronic tension-type headache ?
tension headache 15 or more days a month
how would you manage tension type headache?
acute: aspirin, paracetamol or an nsaid - 1st line
prophylaxis: 10 sessions acupuncture over 5-8 weeks
low dose amitriptyline - prophylaxis.
categories of tension headaches
infrequent - less than 1 day per month
frequent - 10 times in less than 15 days a month for more than 3 months
chronic: 15 days or more a month, more than 3 months - no med overuse
what is a cluster headache?
one of most painful .
occur in clusters lasting several weeks.
clusters typically once a yr.
epi of cluster headaches
50-60 yrs
more in males : 3-1
causes of cluster headache
male
smoking
alcohol could trigger
also nocturnal sleep
features of cluster headache
4-12 weeks lasts
pain : intense sharp stabbing pain around 1 eye - recurrent attack always same side.
typically once or twice a day - 15min-2 hrs
pt restless and agitated during attack.
redness
nasal stuffiness
lacrimation
lid swelling
miosis (constriction of pupils) and ptosis (drooping of upper eyelid) in minority
how would you investigate for cluster headache?
neuroimaging - underlying brain lesions can be found even if clinical sx are typical for cluster headache
MRI with gadolinium contrast
how to diagnose cluster headache : criteria
at least 5 attacks meeting criteria B-D
b - severe/very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 mins (when untreated)
c - either or both of:
- 1 of following symptoms or signs , ipsilateral to headache:
- eyelid oedema
- forehead and facial sweating
- miosis and/or ptosis
- nasal congestion and/or rhinorrhoea
- conjunctival infeciton and/or lacrimation - sense of restlessness or agitation
d. - frequency between 1 every other day and 8 per day.
e - no better diagnoses.
how to manage cluster headache?
acute: 100% oxygen (80% response rate within 15 mins), subcut triptan (75% response rate within 15 mins)
prophylaxis:
verapimil
some say tapering dose of prednisolone
