Dunedin-Neurology Flashcards
How to diagnose Parkinson’s disease?
2 of the 3 features:
Bradykinesia + resting tremor OR rigidity
What are some motor symptoms in parkinsons that are not levodopa responsiveness?
voice change
freezing
gait ignition failure
What are the key prodomal features of parkinsons?
*RBD (REM sleep behaviour disorder) –> movements of body or limbs associated with dreaming with at least one of the following
- potentially harmful sleep behaviour
- dreams that appear to be acted out
- sleep behaviour that disrupts sleep continuity
*hyposmia
*anxiety
* constipation
What are some mutations related to Parkinsons disease?
GBA (glucocerebrosidase)
LRRK2
Describe the order of pathological changes in PD
starts in the medulla, and the olfactory bulb, then spreads upwards to substantial nigra, then finally into the cortex
Where is levodopa absorbed? What is the half life.
absorption in duodenum and jejunum. it competes with amino acids for gut absorption
therefore relies on gastric emptying.
half life 1.5 hours
What can cause increased plasma concentration/dose of levodopa?
advanced age
low body weight
What are some S/E of levodopa?
nausea
orthostatic hypotension
hallucinations
sleepiness and sleep attacks
confusion
motor fluctuations and dyskinesia
contributes to impulse control disorders
What are some medications for the treatment of PD?
What is the MOA of dopamine agonist in parkinsons disease?
directly stimulate the post-synaptic dopamine receptors
longer half life than levodopa
but less potent and greater S/E than levodopa
e.g. apomorphine, pramipexole, ropinirole, rotigotine, piribedil
What are S/E of dopamine agonist?
*nausea
*orthostatic hypotension
*confusion and *hallucinations
*sleepiness/sleep attacks
*peripheral oedema, ankle swelling, facial oedema
*skin irritation/rash (rotigotine)
*impulse control disorders
How to manage impulse control disorders when using dopamine agonists?
reduce or change dopamine agonist
this is associated with things like pathological gambling, hypersexuality, compulsive (binge) eating, compulsive shopping
What is punding?
often due to taking too much dopamine
often associated with marked dyskinesias and off-state dysphoria and with over-use of levodopa
mx: reduce levodopa
What is the MOA of MOA inhibitors such as rasagiline
prevents apoptotic cell death
irreversible inhibitor
MAO-type b- 80% of all MAOs in the brain
half life is 40 days
What is “wearing off” in parkinsons disease using Levodopa and how to treat?
Dose starts to wear off
treat:
* add entacapone or rasagiline
*decrease dose intervals
* increase levodopa dose size
* add dopamine agonist
Describe levodopa-induced dyskinesia
Peak dose: 30-60 min after levodopa, mainly chorea, entire body or upper half, person not aware
Treat: reduce levodopa dose size, add amantadine, add dopamine agonist and reduce levodopa, stop entacapone
End of dose: 3-4 hours post levodopa, or early morning, dystonia, often foot/leg, often painful
Treat: add entacapone or selegiline, decrease dose interval, increase levodopa dose size, add amantadine, add dopamine agonist
What are COMT inhibitors and difference between them and S/E
prolong action of levodopa
entacapone and tolcapone
tolcapone more likely to cause liver problem however it can cross blood brain barrier
S/E: insomnia, lived reticular, confusion, leg oedema, blurred vision
What is treatment of RBD (rapid eye movement sleep disorder)?
1) clonazepam
2) melatonin
3) small case series suggest: Pramipexole, donepezil, cannabinoids
How to treat dementia in parkinsons disease
Cholinesterase inhibitor:
- rivastigmine ,donezpezil
memantine
How to treat psychosis in Parkinson’s?
Benign hallucinations –> don’t treat
Paranoid psychosis –> quetiapine, reduce PD drugs, cholinesterase inhibitors (donepezil) if dementia/confusion, clozapine if ongoing psychosis
What are some advanced therapies for Parkinsons disease?
*apomorphine subcutaneous infusions
* DuoDopa Gel via PEG-J placement
*pallidotomy
* deep brain stimulation
What is the selection of patients for deep brain stimulation in Parkinson’s disease
1) typical PD and levodopa-responsiveness
2) medically healthy
3) No dementia
4) no psychosis or severe hallucinations
5) <70 years
What is the difference between MSA-C and MSA-P?
Automonic dysfunction + motor features (parkinsonsism or ataxia)
MSA-C: multiple system atrophy, the cerebellar predominant form (nystagmus, dysarthria, ataxia)
MSA-P: the parkinsons predominant form (symmetric rigidity, little tremor, poor postural reflexes)
- erectile failure, urinary incontinence, postural hypotension
What do you see in the brain for Multiple system atrophy?
alpha synucleiopathy
hot cross bun sign: atrophy of pons and cerebellum
MCP atrophy
putaminal rim sign
increased diffusion putamen
Is Progressive Supranuclear palsy a tauopathy?
Yes
neurofibrillary tangles (made up of tau) in brain stem, flame-shaped NFTs, coiled bodies, neuronal loss and gloss
What are the types of PSP?
1) Richardson’s syndrome: classic features of PSP early onset falls, slow vertical saccades, supra nuclear vertical gaze palsy, postural instability, frontal dementia, axial rigidity
2) PSP-parkinsons: asymmetric onset, tremor, response to levodopa, better prognosis
What is the radiological sign of PSP?
hummingbird or ‘kind penguin’ sign ie mid brain atrophy
Is Corticobasal syndrome a tauopathy?
yes
What is a common presentation of corticobasal syndrome?
rigid jerking arm
apraxia, frontal lobe dementia
+/- supra nuclear gaze palsy but not as severe as PSP
What are core features of dementia with Lewy bodies?
dementia has to start before or within a year of motor symptoms
core features (need 2)
a) fluctuating cognition
b) recurrent visual hallucinations
c) parkinsonsim
Suggestive
a) REM sleep behaviour disorder
b) severe neuroleptic sensitivity
What chromosome is the Huntingtin gene on?
Chromosome 4
CAG repeat (>40 repeats for sure, 36-39 increased risk, 6-25 unaffected)
What are the main features of Huntingtons disease?
1) involuntary movements (chorea, dystpnoa and Parkinsonism)
2) Behavioural disorders
3) cognitive impairment and dementia
Age of onset is based on size of CAG repeat expansion. True or false?
True
Treatment of Huntington?
symptomatic:
atypical antipsychotics
- tetrabenazine
- risperidone, olanzpine
- aripriprazole
antidepressants
What is the diagnostic criteria for restless legs syndrome?
1) an irresistible urge to move the legs, usually but not always accompanied by uncomfortable and unpleasant sensations in the legs
2) Worse during rest or inactivity
3) symptoms partially or totally relieved by movement
4) worse in evening or night
5) no other conditions (myalgia, venous stasis, leg oedema, arthritis, leg cramps, positional discomfort, habitual foot tapping)
Describe anti-LGL1 encephalitis
a type of limbic encephalitis
faciobrachial dystonic seizures
How to treat NMDA receptor antibody-mediated encephalitis?
corticosteroids
IVIG
plasma exchange
rituximab
cyclophosphamide
What are common features of limbic encephalitis?
memory impairment
Describe common types of limbic encephalitis
LGL1 (most common)- hyponatraemia, faciobracial seizures
GABABR and AMPAR
What is the MRI finding in limbic encephalitis
Mesial temporal lobe hyperintensty
What are the characteristics of DPPX antibodies encephalitis?
onset subacute to chronic
weight loss and GI symptoms
cognitive dysfunction
CNS hyper excitability (hypereflexia, myoclonus)
ataxia
eye movement disorder
What is Lhermitte’s and Uhthoff’s symptoms?
Lhermittes: transient sensation of an electric shock that extends down the spine and extremities upon flexion and/or movement of the neck.
Uhthoff: transient worsening of neurological function lasting less than 24 hours that can occur in multiple sclerosis patients due to increases in core body temperature
What are the types of multiple sclerosis?
What is the best imaging for MS?
MRI
GAD enhancement shows up “active lesions”
What is the characteristic appearance of MS on neuroimaging?
– periventricular, corpus callosum, centrum semiovale
– radiating out from corpus callosum = Dawson’s fingers
– brainstem, cerebellum
– hyperintense on T2 & Proton Density (PD) sequences
– hypointense on T1 (black holes) = axonal damage
What does ring-like enhancement suggest in MS lesions?
peripheral inflammation & complete central demyelination ( = reactivation at periphery of a chronic lesion).
What are things we can use in the diagnose of MS?
*MRI
*Evoked potential (EPs)
*Central motor conduction time (CMCT)
*Lumbar puncture - CSF- oligoclonal bands +ve in CSF but NOT In serum. Increased CSF IgG synthesis
What are some Multiple Sclerosis mimics?
*NMOSD & MOGAD
*Inflammatory disease (SLE, Sjogrens, PAN, Behcets etc)
*Infectious disease
*Granulmonatous disease
* diseases of myelin
*CADASIL
What is true about pregnancy in MS?
relapse rate reduced during pregnancy, especially in 3rd trimester
increase in relapse rate in 6 months after delivery
breastfeeding decreases early relapse rate
What are poor prognostic factors of MS?
Male
>40 years
What are MRI features that suggest poor prognosis of MS?
*high T2 lesion load
*>2 GAD enchanting lesions
*>T1 hypointense lesions
*early atrophy
* infratentorial as opposed to supratentorial lesions
Describe the treatment of MS
Acute: methylpred. Avoid pred in optic neuronitis
Continuous
- low efficacy: IFN, GA (glatiramer acetate), teriflunomide
- medium efficacy: S1PR (sphingosine-1-phosphate receptor eg ozanimod, pronesimod), DMF (dimethyl fumarate)
- high efficacy: Natalizumab (akpha-4-integrin blocker), B cell therapies (ocrelizumab, ofatumumab)
- alemtuzumab anti-cd52 is used but less often
Pulse
- medium efficacy: cladribine
- high efficacy: alemtuzumab, HSCT
What are side effects of alemtuzumab (CD52)
Profound depletion of T cells (for >1 year), profound depletion of B cells
autoimmune thyroid disaese
Immune mediated conditions including hepatitis and haemophagocytic lymphohistiocytosis, bleeding in lungs, MI, stroke, arterial dissection and severe neutropaenia
What is the MOA of fingolimod?
Decreases ability of lymphocytes to enter CNS by preventing the
egress of lymphocytes from lymphatic tissues.
Down regulates four sphingosine-1-phosphate receptor subtypes
What is the MOA of teriflunomide?
Inhibits pyrimidine synthesis (dihydroorotate dehydrogenase inhibitor)
a metabolite of leflunamide
S/E: HTN, LFT and RBS abnormal, alopecia and diarrhoea
Is stem cell transplant an option for MS?
Possibly
What antibodies occur in neuromyelitis optica spectrum disorder (NMOSD)
aquaporin 4 abs
in high conc in foot processes of astrocytes along endothelial lining of blood brain barrier
pathology: complement mediated destruction of astrocytes with secondary demyelination
What are spinal cord MRI abnormalities noted in NMOSD?
longitudinally extensive (>3 segments) spinal cord MRI abnormalities
(LETM= longitudinally extensive transverse myelitis)
often have optic nerve disease
What is the CSF like in NMOSD?
significant pleocytosis
What is the pathophysiology of NMOSD?
complement mediated destruction of astrocytes with secondary demyelination
What antibody is involved in Myelin Oligodendrocyte Glycoprotein Associated Disease (MOGAD)?
anti-MOG
What are some symptoms of MOGAD?
Optic neuritis and transverse myelitis
What is the pathophysiology of MOGAD?
Oligodendrocyte directed pathology = Oligodendrocytopathy
What are the greatest risk factors for ischaemic stroke? Haemorrhagic stroke?
Ischaemic:
1) Age
2) Hypertension
3) Atrial fibrillation
Haemorrhagic
1) HTN
2) cerebral amyloid antipathy
Describe the cerebral circulation
What is Gerstman syndrome?
location: inferior parietal lobule of dominant hemisphere
Dysgraphia/agragraphia
dyscalculia/acalculia
finger agnosia
left-right disorientation
+/- aphasia
+/- apraxia
What is lateral medullary syndrome?
AKA Wallenberg syndrome AKA PICA syndrome AKA vertebral artery syndrome
Location: lateral medulla
Vessels: vertebral artery, PICA, superior middle and inferior medullary artery
Symptoms:
*contralateral trunk/limb numbness (pain/temp)
*ipsilateral facial numbness
*skew deviation/room tilk
* dysphagia/hoarseness/gag
*horners syndrome
*Limb ataxia
*Palatal myoclonus
* vertigo/nystagmus
What is the top of basilar syndrome?
AKA Ponto-mesencephalic stroke
symptoms:
*Ptosis
*dilated pupils
*ocular motor deficits
*somnolence, hallucinations, dreamlike behaviour
*motor function otherwise preserved
What is Anton syndrome?
stroke syndrome
bilateral occipital lesions, cortical blindness
What is Benedikt syndrome?
Midbrain stroke, posterior cerebral artery or penetrating branches of basilar artery, CN III palsy, ataxia/choreoathetosis
What is Balint syndrome?
B/L parietal/occipital junction lesions: e.g. watershed
simultagnosia
oculomotor apraxia
optic ataxia
What is anterior spinal artery syndrome?
loss of power distally (usually up to thoracic) +/- loss of temp/pain
posterior column unaffected
What is the BP target in ICH?
SBP 140
Where is surgical intervention relevant in ICH?
posterior fossa
What is the work-up for subarachnoid haemorrhage?
*Head CT with CTA
*lumbar punture for xanthrochromia
*MRI with SWI
What is the treatment of subarachnoid haemorrhage?
*Lower BP <140
*clip/coil aneurysm to fix the underlying problem
*oral nimodipine to prevent vasospasm
Describe the timing of IV thrombolysis and ECR for stroke
IV thrombolysis: <4.5 hours (or 9 if small core)
Endovascular thrombectomy: <6-7 hours (or 24 hours if small core and mismatch volume >15ml)
extended window possible using advanced imaging
What vessels can we access with ECR?
ICA and M1
M2
ACA and PCA
Basilar
What are contraindications for tPA
- known hx of ICH
- prior stroke or serious head injury within 3 months
- sustained BP >185/110
-dabigatran within 48 hours - heparin within the last 48 hours
- major surgery within past 14 days
Describe herniation syndromes
What is is most significant risk factor for stroke?
hypertension
What is the LDL target in stroke?
<1.8
When do you do a Carotid endarterectomy?
if symptomatic AND
ipsilateral 70-99% stenosis
some evidence for 50-69% stenosis
What anti-seizure medication work on inhibitory synapses vs excitatory synapses?
Excitatory synapse:
- Phenytoin, carbamezapine, valproid acid, lamotrigine, topiramate, oxcarbezine
- levetiracetam
- topiramate
- felbamate
- gabapentin/pregabalin
Inhibitory synapse:
- benzodiazepine
-topiramate
- barbiturates
- vigabatrin
What is the MOA of levetiracetam?
synaptic vesicle protein 2A, inhibition Ca current
95% really excreted
S/E- irritability, mood swings
What is the MOA of Perampanel (Fycompa)
glutaminergic AMPA antagonist
adjunctive for focal seizures
What is the role of vagus nerve stimulation?
role in medically refractory epilepsy
Describe HLA related to carbimazole
HLA B1502 –> CBZ induced SJS
HLA A 3101 –> CBZ induced rash
Which anti-eleptics are teratogenic?
phenobarbitone
valproate
What is an adverse reaction with using lamotrigine and valproate together?
Rash
What is the adverse effects with OCP and lamotrigine?
reduced Seizure control
What is the adverse effect carbamazepine to warfarin?
reduced INR
What are some antibodies involved in autoimmune epilepsy
What are common causes of multiple mononeuropathies?
Diabetes
vasculitis
leprosy
sarcoidosis
demyelinating neuropathies
heredity liability to pressure palsies
neurofibromatosis
entrapment/compressive neuropathies
multifocal mononeuropathy with conduction block (MMNCB)
Describe large vs small nerve fibres
Small fibres: pain and temp
larger fibres: motor & JPS, vibration
What are some causes of pure sensory neuropathy?
diabets
b12 deficiency
HIV
amyloidosis
Sjogrens syndrome
sarcoid
paraneoplastic
pyridoxine (vit B6) intoxication
hereditary causes
What part of the neuron is involved in axonal pathology vs demyelination?
axon= axonal pathology
Schwann cell= demyelination
What infection is related to GBS?
campylobacter jejuni
What is the management of demyelinating neuropathies?
plasmapharesis
IVIG
Steroids (not for GBS)
immunosuppression
What is pet cavus
What is “stork leg”
long standing problem
What are the subtypes of hereditary neuropathy
- HMSN 1 - Demyelinating
- HMSN 2 - Axonal
- CMT1X - x-linked
- CMT4 – autosomal recessive types
What does the CSF show in paraneoplastic sensory neuropathy?
increased protein
pleocytosis (<100 cell/dl), lymphocytes
OCBs positive, IgG ratio abnormal
Describe GBS/AIDP
- progressive limb and cranial nerve weakness over days
- relative symmetry of weakness
- sensory loss, dysesthesia, pain
- loss or decreased deep tendon reflex
- dysautonomia- HR, BP lability
- resp and bulbar impairment
- previous acute illness (diarrhoea- c jejuni)
- monophonic illness
What are the investigations for GCS/AIDP and what does it show?
NCS- demyelination, prolonged F waves, prolonged distal motor latencies, slowing NCVs. NCS may be relatively normal in the beginning.
CSF- raised protein, acellular or <10wbc
What are some GBS/AIDP variants?
Acute motor axonal neuropathy (AMAN)
- associated with ganglioside GM1 antibodies
Miller Fisher syndrome (MFS)
- ophthalmoplegia, ataxia, areflexia, Gq1b abs
Treatment of GBS/AIDP?
IVIG, plasma exchange (can get autonomic instability)
NOT steroids
What are the characteristics of CIDP?
relapsing ongoing symptoms (proximal and distal weakness, decreased to loss DRTs, autonomic features, variable sensory features, rarely papilloedema)
CSF: raised protein, <10 wbc
What is the treatment of CIDP?
steroids, IVIG, rarely PLEX in early severe cases, mycophenolate, azathioprine
What antibodies are associated wth multifocal motor neuropathy?
possible GM1 antibodies
What antibodies are associated with DADS (distal acquired demyelinating sensory Ny)
anti-MAG antibiotics
might mention paraprotein
Which antibodies are associated with paranodopathies?
Neurofascin NF155, contactin 1
What is POEMS? And treatment
polyneuropathy, organomagaly, endocrinopathy, IgM paraprotein, skin changes
often have sclerotic bone lesions and elevated VEGF levels
management: lenalidomide, bortezomib, melphalan
What are the antibodies related to myasthenia gravis? HLA association
AChR (80%), MuSK antibodies (20%)
LPR4 (generalised or ocular)
Agrin (Gen>ocular)
Collagen XIII (Gen)
HLA DR14- DQ5 association
What conditions is myasthenia gravis associated with?
Hyperthyroidism, SLE, Scleroderma, RhA
What is the typical phenotype for MuSK Mg?
severe facial and bulbar weakness with atrophy of affected muscles.
Limb muscles often less affected
tend to be milder
What is Simpsons test?
a test in ocular MG , drooping of one upper lid when looking up
Describe the treatment of MG
*Acetylcholinesterase inhibitors (pyridostigmine)
* steroids (prednisone)
* steroid sparing agents: azathioprine, mycophenolate mofetil
Efgartigimod
Rozanolixizumab
ravuluzimab
zilucuoplan
eculuzimab
rituximab
How to treat myasthenia crisis?
ICU
treat infection if present
increase prednisone
plasma exchange or IVIG
thromboprophylaxis
What is the main paraneoplastic cause of Lambert eaton myasthenia gravis?
SCLC
What is the pathophysiology behind Lambert eaton myasthenia gravis?
IgG antibodies against voltage-gated calcium channels
What is the clinical presentation of Lambert eaton myasthenia gravis?
Mainly proximal disease
worse in lower limbs
not usually fatiguable
distal symmetrical sensory neuropathy
autonomic neuropathy (dry mouth/eyes and impotence)
reflexes depression, but potentiate as does power
bulbar weakness and diplopia less common
What is the treatment of Lambert eaton myasthenia syndrome?
potassium channel blocker (3-4 diaminopyridine)
immunosuppression
successful treatment of cancer
What are some clinical tests for MG?
Ice Pack test
- put on ptosis, painful, however improved neuromuscular transmission at lower temperatures
- sensitivity 80%
Tensilon test
- short acting acetylcholine esterase inhibitor
- target muscle, inject, reassess at 1 minute
- can get false positive like MND
- can cause Brady
Discuss brachial plexus
What is brachial neuritis?
AKA neuralgic amyotrophy/Parsonage Turner syndrome/inflammatory brachial plexopathy
can be seen post infection/vaccination
clinical presentation: severe shoulder pain at onset, followed by weakness and wasting often around shoulder girdle. sensory loss often outer upper arm.
winging of scapula.
What is neurogenic thoracic outlet syndrome?
a cause of brachial plexus injury
fibrous band over lower trunk brachial plexus
insidious onset pain and sensory loss/paraestheisae
positional
“punched out”
What nerve does shoulder dislocation affect?
suprascapular nerve affecting infraspinatus and supraspinatus
axillary nerve: deltoid, teres minor
sensory loss deltoid
brachial plexus injury
Describe Ulnar vs C8 root problem
Motor:
- Ulnar: all muscles except LOAF
- C8 root: all muscles including LOAF (responsible for flexion)
LOAF:
lateral two lumbricals.
opponens pollicis.
abductor pollicis brevis.
flexor pollicis brevis.
Sensory: more sensory loss with C8
Describe the sensory distribution of the hand
What is a common antibody in paraneoplastic neuropathy?
Anti-Hu
What is the treatment for trigeminal neuralgia?
Carbamezapine , Gabapentin, lamotrigine, surgical decompression
What is Foster Kennedy Syndrome?
- Olfactory groove meningioma
- Ipsilateral anosmia, ipsilateral visual loss and optic atrophy
- Contralateral papilledema
What is neuralgia paraesthetica?
- Pain/dysesthesia affecting anterolateral thigh due to compression of lateral femoral cutaneous nerve (inguinal ligament
Describe features of femoral neuropathy
- Hip flexion and knee extension weakness
- Absent patellar reflex
- Sensory loss anterior thigh and medial lower leg
Describe ankle movements, nerves involved and muscles involved.
Ankle movements
- Dorsiflexion: tibialis anterior, deep branch of peroneal (L4,L5)
- Eversion: peroneus longus, superficial branch of peroneal (L5,S1)
- Inversion: Tibialis posterior, tibial nerve (L4,L5)
- Plantarflexion: gastrocnemius and soleus, tibial nerve (S1, S2)
Peroneal nerve: up and out
Tibial nerve: Down and in
What drug induced neuropathy does ethambutol cause?
optic neuritis
What drug-induced neuropathy does nitrous oxide cause?
B12 deficiency
o Subacute combined degeneration of spinal cord
o Increase homocysteine and MMA
What drug-induced neuropathy does anti-TNFalpha cause?
CNS +/- PNS demyelination
What is onion bulb histology?
Seen in Charcot-Marie Tooth syndrome, also seen in CIDP
Describe the neuronal antibodies
What are F wave and H reflexes?
o F wave: a late motor response elicited by the backfiring of motor neurons after supramaximal electrical stimulation of a peripheral nerve
o H reflexes: involves both sensory and motor nerves. It is elicited by stimulating a sensory nerve (e.g., tibial nerve), which triggers a reflex response in the corresponding motor nerve.
Describe the timing of motor vs sensory loss after injury
- Motor > sensory
- Motor by day 3, sensory by day 5
Describe NCS: normal conduction values, latency, amplitudes
Conduction velocity
o UL 50-60ms
o LL 40-50ms
Latency
o <4ms
Amplitudes
o Sensory >6uV
o Motor >4 uV
Describe changes in neuropathy vs myopathy
Describe antibodies associated with classic paraneoplastic syndromes (neruology) and their treatment
Hu
CRMP5
Ma2
amphiphysin
treatment: anti-T cell –> rituximab, cyclophosphamide
Distinguishing between types of limbic encephalitis
GABAAR- refractory status epilepticus
CASPR2- peripheral-nerve hyperexcitability, neuropathic pain
DPPX- hyperekplexia, myoclonus
What can you use is tuberous sclerosis that are high risk for seizures?
mTOR- everolimus and sirolimus
Causes of motor only neuropathy?
motor neuron disease
poliomyelitis
lead
botulinism
drugs (vincristine, dapsone, amiodarone)
What is the role of neurofascin antibodies?
For paranodopathies (form of CIPD), especially if patient resistant to usual CIPD treatments (steroids and or IVIG)
What are genes associated with migraines?
KCNK18 and CSNK1D genes
What is the treatment of a migraine?
Acute: anti-emetic (IV prochlorperazine), triptan
Status migrainous –> SC sumatriptan or IV ketoralac or IV chlorpormzine
Prophylaxis
- Insomnia –> TCA, pregabalin, gabapentin, propranolol, candesartan, topiramate
Compare the different headaches syndromes
