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MED627 > Tumour/Headache > Flashcards

Tumour/Headache Flashcards

1
Q

how many types of brain tumours are there and how are they divided into groups?

A
  • over 150 types

- divided into groups based on the cell or region they are derived from e.g. meninges (meningioma), glial cells (glioma)

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2
Q

which are regions in the brain where there could be a tumour or the different types of tumour?

A
  1. meninges - meningioma
  2. sellar region - craniopharyngioma: benign, cystic tumours
  3. germ cell tumours - rare paediatric, dually cancerous tumours in pituitary/ pineal gland
  4. gliomas (on the brain cell) - oligodendglial cells, astrocytic cells, ependymal cells, neuronal tumours
  5. cranial nerves (schwannoma) e.g. eight nerve acoustic neuroma (deafness)
  6. haematopoietic - lymph cells - primary CNS lymphoma
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3
Q

what are secondary tumours? give examples

A

tumours that spread from organ to brain or metastasis, also called metastatic tumours e.g. lung, breathing, colorectal, testicular, renal cell, malignant melanoma

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4
Q

what is TNM system and why it not used to classify brain tumours?

A
  • tumour node metastatic (TNM) system is used classify the tumours spreading from one organ to another however, the tumour cannot spread to other organs from the brain
  • therefore, the WHO classification is used to classify brain tumours
  • WHO classification is based on histology (cell type)
  • tumours are graded using morphology into four groups of malignancy
  • I - most benign an IV - most malignant
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5
Q

what is the new WHO classification based?

A
  • earlier WHO classification was based on histological features only
  • However, WHO classification 2016 combines histological features along with molecular genetic features
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6
Q

what are gliomas? and how are they graded?

A
  • tumour of glial cells (astrocytes/oligodendrocytes/ependymal cells)
  • most common primary brain tumour
  • WHO grade I and II - low
  • WHO grade III and IV - high
  • grade 1 - 99% stay the same
  • grade 2 - initially benign but eventually grow and tun malignant
  • grade 3 and 4 - malignant
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7
Q

on what basis on the tumours characterised histologically?

A
  1. Cellularity
  2. mitotic activity
  3. vascular proliferation
  4. necrosis
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8
Q

what are the survival rates of grade 2,3 and 4 gliomas?

A

2 - 10 year average
3 - 3.5 years
4 - 12 months/1 year

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9
Q

what is LGG grade 11, the median affecting age and its survival rate?

A
  • median age - 35 years
  • Slow growing but will undergo anaplastic transformation (malignant)
  • the transformation time will depend on the cell of origin
  • for e.g. Astrocytomas – 3-5 years, Oligodendroglioma – 7-10 years
  • therefore, the patient with oligodendroglioma might have a longer life compared to a patient who has astrocytoma
  • nevertheless, survival time longer than de novo HGG
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10
Q

what are the factors influencing the prognosis of LGG?

A
  • Histology type
  • Age *
  • Size of tumour *
  • Rate of growth
  • Location *
  • Cross midline
  • Presenting features
  • Performance status *
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11
Q

what are HGG (III and IV) and what is mediate age of onset

A
  • most common type of brain tumour
  • 85% of all new causes of malignant primary brain tumour
  • either as primary tumour or from pre-existing low grade
  • median age of onset for
    III - 45 years
    IV - 60 years
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12
Q

what is the prognostic value of molecular classification of glioma?

A

??

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13
Q

what are the causes of tumour?

A
  • media coverage: mobile phone usage, high BP, dental x-rays
  • the known causes stated below
  • majority - no cause found yet
  • ionising radiation: for children with leukaemia are high risk of meningioma
  • 5% family history: genetic syndromes like neurofibromatosis, tuberose sclerosis, Von Hippel-Lindau disease
  • immunosuppression e.g. CNS lymphoma via drugs or HIV
  • however, no evidence to link mobile phone usage
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14
Q

what are the symptoms of a brain tumour?

A
  • varied presentation dependent on tumour type, grade and site
  • common symptoms can include headache, seizures, focal neurological symptoms and other non-focal symptoms
    1. Focal (progressive over days – weeks):
  • Hemiparesis: subacute and progressive
  • Hemisensory loss
  • Visual field defect: not easily noticed, comes under attention after automobile accidents
  • Dysphasia
  • ataxia?
    2. Non-focal
    personality change/behaviour, memory disturbance, language difficult mistaken as confusion
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15
Q

how common is headache as symptom for brain tumour?

A
  • woken by headache, worse in the morning, worse while lying down
  • associated w nausea and vomitting (as ICP is elevated), exacerbated by coughing, sneezing, drowsiness
  • 24% - first symptoms
  • 46% - at presentation
  • however, only 2% at hospital presentation have isolated headache
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16
Q

how common is seizure as symtoms for brain tumour?

A
  • common presentation of brain tumour
  • occurs in 25% w brain malignant tumour but
  • presenting symptom in up to 90% w LGG
  • most seizures: focal signature reflecting the location of brain
  • many proceed to secondary generalisation -> all generalised seizures from brain tumour will have a focal onset whether to not it is clinically clear
  • First fit 2-6% = brain tumour
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17
Q

how are the different lobes of the brain involved in seizure?

A
  1. frontal:limb jerking, headache or eye deviation
  2. parietal: sensory disturbance - spreading tingling
  3. temporal: deja vu, jamais vu, memories, feeling. dread, rising feeling
  4. occipital - positive visual disturbance - coloured balls
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18
Q

what other signs to look for in brain tumour?

A
  1. Papilloedema
  2. Focal neurological deficit
    - Hemiparesis
    - Hemisensory loss
    - Visual field defect
    - Dysphasia
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19
Q

what are the red flags of brain tumour?

A
  • headache
    1. with features of raised ICP (including papilloedema)
    2. with focal neurology- check for field defect
  • other urgent referrals
    3. new onset focal seizure
    4. rapidly progressive focal neurology (w/o headache)
    5. past history of other cancer
  • noteworthy, brain tumour is unlikely the diagnosis if long history of isolated headache
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20
Q

what is the difference in presentation of LGG and HGG?

A

low grade - typically present w seizure (could be incidental finding)
high grade - rapidly progressive neurological deficit (weakness on one side), symptoms of raised ICP (swelling?)

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21
Q
  • significance or neuroimaging in detecting brain tumour (CT vs MRI)
  • presentation of different tumour on scans
  • what are the modern imaging techniques and its uses
  • and when should biopsy be performed?
A
  • neuroimaging only test necessary to diagnose a brain tumour
  • suspected brain tumour: MRI w gadolinium contrasts
  • CT(w contrast) for those who cannot under MRI (e.g. pacemaker)
  • Malignant brain tumour (primary or metastatic): enhance w Gd, may have central necrosis, surrounded by edema, high grade:irregular mass with vasogenic oedema
  • LGG: typically don’t enhance w Gd, best predicted w FLAIR IMR
  • meningioma: characterstic MRI appearance (dural tail and compress but do not invade the brain) [noteworthy: dural metastases or dural lymphoma can have having similar appearance)
  • imaging useful for most primary and metastatic tumour but occasionally diagnostic uncertainty
  • then, brain biopsy may be helpful to identify the definitive diagnosis
  • however, when tumour strongly suspected -> biopsy obtained as intraoperative frozen section before resection
  • fMRI: presurgical planning
  • PET: metabolic activity of lesion seen on MRI
  • MR perfusion + spectroscopy: blood flow, tissue composition
  • these techniques may help distinguish tumour progression from necrotic tissues (??) or identify HGG and LGG
  • MRI better than CT
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22
Q

what is the treatment for brain tumour and over all survival area?

A
  • Depends on tumour type, grade and site
  • Treatment is non-curative (except for grade I)
  • only 19% survive 5 years or more.
  • only 14% of all brain tumours survive 10 or more years
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23
Q

what is the treatment for HGG and rate of prognosis with no treatment or after treatment?

A
  1. steroids – reduce oedema
  2. surgery – biopsy or resection for tissue diagnosis, relief of raised ICP, prolongation of survival
  3. Radiotherapy – mainstay of treatment. Radical vs palliative
  4. Chemotherapy – Temozolamide, PCV
    - Prognosis - 6 months no treatment /18 months with
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24
Q

what is the treatment for LGG?

A
  1. Surgery – early resection or biopsy - does not cure but prolongs survival. despite of no evidence on scan some cells still remain after surgery
  2. Radiotherapy alone – delays disease transformation not overall survival
  3. Radiotherapy and Chemotherapy – evidence improves long-term survival
    - add details of RTOG 9802
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25
Q

what is awake craniotomy and its results? r

A

w mapping

w/o mapping

26
Q

how commonly is headache presented at hospitals?

A
  • headache is a common clinical presentation
    GP - 4.4 consultations per 100 registered patients
    Neurologist - 25% referral
    A+E - 1-2% acute presentations
27
Q

what are the most common causes of headache?

A 
primary headache
- tension type: 70%
- migraine: 16%
- cluster headache 
secondary headache
- systemic infection: 63%
- head injury: 5%
- vascular disorder: 1%
- SAH: <1%
- brain tumour: 0.1%
28
Q

why is headache more common in female?

A
  • Migraine: predominantly female disorder: 15% women and 6% men over 1yr period
  • Menarche, menstruation, pregnancy, menopause, and the use of hormonal contraceptives and hormone replacement treatment may influence migraine occurrence.
  • occurs at menarche, before or during menstruation, and ameliorates during pregnancy and menopause.
  • Those variations are mediated by fluctuation of estrogen levels through their influence on cellular excitability or cerebral vasculature.
  • Moreover, administration of exogenous hormones may cause worsening of migraine as may expose migrainous women to an increased risk of vascular disease.
  • In fact, migraine with aura represents a risk factor for stroke, cardiac disease, and vascular mortality.
  • Studies have shown that administration of combined oral contraceptives to migraineurs may further increase the risk for ischemic stroke.
  • Consequently, in women suffering from migraine with aura caution should be deserved when prescribing combined oral contraceptives
    Sacco et al. 2019
29
Q

what is the classification of headache?

A

according to the international classification of headache disorders third edition

  1. primary: independent disorder not caused by another disease or trauma
  2. secondary: headache is a symptom of underlying disease or injury that needs to be treated
  3. cranial neuralgias: Headache that occurs due to a sudden burst of activity in sensory cranial nerves, predominantly the trigeminal nerve.
30
Q

where do feel the pain in headache (anatomy and physiology of headache)?

A
  1. peripheral nociceptors (ascending and descending pathways) stimulated in response to tissues injury, visceral distension or other factors
  2. CNS/PNS pain producing pathways when damaged or activated inappropiraitely
    - headache may originate from either or both mechanism
  3. key structures involved in primary headache
    a. trigeminal nerve innervating the large intracranial vessels and dura matter by (trigeminovascular system)
    b. trigerminal nerve innervating the upper cervical trigeminocervical complex
    c. rostral pain processing regions like ventroposteromedial thalamus and the cortex
    - further, the brain relies on attention, context, emotion and mood for pain perception e.g. anticipation and anxiety can also influence the pain so a person might give a higher score of pain than the first time
31
Q

what was the vascular theory of migraine and what are its limitations?

A
  • studies in mid 20th century suggested migraine had a vascular aetiology since the patients described it as a throbbing pain
  • Therefore, they stimulated vessels and relied on the response, this would be unethical atm, won’t get ethics approval
  • however,
32
Q

what was the theory of cerebral blood flow of migraine and its limitations?

A
  • studies in late 20th century suggested migraine was associated with the CBF - hypo- or hyperperfusion
  • however, the onset and termination of pain did not correlate with the change in blood flow
  • highlighting it is not related blood flow and blood vessels
33
Q

what are the criteria for the diagnosis of migraine w/o aura?

A
  • 5 attacks fulfilling the criteria listed below
    1. attacks last 4-72 hours (3days)
  • episodic migraine - pain comes and goes off
  • most people have episodic instead of chronic headache
    2. 2 of the following: unilateral, pulsing, moderate/severe, aggravation by routine physical activity
    3. either nausea and/or vomiting or photophobia and phonophobia during the headache
  • not attributed to another disorder
  • anxiety when they move around -> prefer sitting
  • sensitive to light and sound -> prefer to lie down in a dark room
  • some of these symptoms are prevalent in meningitis, however, no infection is found in headache
34
Q

how has the pathophysiology of migraine changed over the years?

A
  • used to be considered as a “vascular headache” in the mid 20th century, however, vascular changes do not explain all migraine features
  • vascular changes was associated due to the description of throbbing pain by patients but 1/3 of patients don’t have a throbbing pain
  • further, headache can be evoked by
    1. lesions or electrodes in breath periaqueductal grey in the absence of vasodilation
    2. stimulation of insular cortex in absence of vascular change
  • migraine is now considered a disorder of brain excitability (ascending, descending pathways, problems with the neural processes)
  • vasodilation may occur as result of the disorder but is not a causative factor migraine pain
  • vasoconstriction may be more important than vasodilation as an initial trigger for migraine symptoms
35
Q

what is the significance of genetics in migraine?

A
  • Twin studies have demonstrated the importance of genetics MZ>DZ
  • been proposed migraine is genetic disorder with channel mutations
  • several rare familial hemiplegic migraine genes have been found
    FHM1 – Ch 19, Calcium channel
    FHM2 – Ch 1, Sodium/Potassium-ATPase
    FHM3 – Ch 2, Sodium channel
  • Even though environmental factors like stress play a role there is genetic factor as well
  • twin has migraine -> more likely for the other twin to get it as well
  • Similarly, with your grandparents and parents -> more likely -> but not mendelian inheritance like autosomal dominant or recessive rather more than one gene
  • Studies have been going from the past 10 years or more but apart from the hemiplegic we haven’t cracked the general
36
Q

what are the theories concerning the initiation of headache/pain?

A
  1. Central mechanisms activate peripheral nociception that initiates pain?
    - unknown mechanisms activate deep brain structures
    - deep structures activate the sensory nerves around the head
    - sensory nerves become sensitised due to local release of signal molecules
    - sensory nerve activation causes pain
  2. Cortex (via CSD) activates trigeminal nerve afferents ?
  3. Brainstem is the migraine generator?
  4. Sterile neurogenic inflammation?
    - but inhibitors of neurogenic protein extravasation clinically not effective
    - Sterile inflammation of meninges – instead of meningitis – something that cause inflammation but not infection – proteins studied on the surface -> release causes neuro-chemical meningitis – drugs targeting those didn’t work in humans
37
Q

how does aura initiate migraine?

A
  • The aura is associated w cortex, animal and human studies have shown that visual aura changes are associated with the cortex whether it is initiation, driving or epiphenomenon is unknown
  • 1940’s - spread of visual aura in relation to occipital cortex calculated at ~3mm/min
  • Visual field gets bigger and bigger and then reduces and comes back
38
Q

what is the significance of spreading depression activity in cerebral cortex?

A
  • An experiment in 1994 studied rabbits under anesthesia and an electrical or mechanical stimulation of cerebral cortex elicited a characters response designated as ‘spreading depression’
  • depression spread out slowly, in all directions, from the region stimulated, so that increasingly distant parts of the cortex were successively involved. similar to doppler effect.
  • cortical waves have been seen in migraine w aura and w/o aura
39
Q

what is cortical spreading depression theory and what’s are its limitations?

A
  • in animal models of migraine it is a propagating wave activity (depolarization of neurons and glial cells) followed by reduced activity that spreads across cerebral cortex.
  • The spreading of this wave is hypothesized to activate the trigeminal nerve afferents, causing inflammatory changes in pain-sensitive structures that create migraine headache.
  • further, it spreads with characteristics that are very similar to clinical symptoms and PET and MRI changes of migraine seen in humans
  • However, classical EEG finings of CSD rarely seen in humans and most patients do not have neurology expected with classical CSD
  • Therefore, migraine may involve waves that are related but not identical to CSD or different types of cortical waves may be produced by distinct cellular mechanisms
40
Q

how have neuro-imaging studies helped us understand the initiation of migraine, migraine w aura and migraine w/o aura?

A

MIGRAINE INITIATION
1. S.K. et al. (2015) showed the ipsilateral pons activation in migraine in PET scans
- they also suggested the lateralisation of migraine pain is due to lateralised brain dysfunction
2. Denuelle et al. (2007) showed hypothalamic activation has been see in migraine in T1 MRI
MIGRAINE W AURA
1. Olesen, et al. 1981 regional CBF – noticed spreading oligaemia
2. Cao et al. 1999
MRI BOLD showed increase then decrease in activity progressing at 3-6mm/min across cortex
3. Hadjikhani et al. 2001 fMRI - increase then decreased signal may be due to increase and decrease in blood flow
4.Bereczki et al. 2008
MRI with DWI showing restricted diffusion in persistent visual aura however, only 20% of people with migraine have visual aura
MIGRAINE W/O AURA
1. Woods et al., 1994
PET and MRI – regional cerebral blood flow was measured during migraine attack and a reduction in rCBF was seen spreading across the cortical surface spanning several major cerebral vessels territory
2. Denuelle et al, 2008
PET used to study blood flow during headache, after headache relief following sumatriptan and during headache free interval. Posterior cortical hypo- perfusion was seen and persisted after sumatriptan injection
3. Chalaupka, 2008
CT during spontaneous migraine without aura showed left temperoparietal hypoperfusion but no change on MRI after 5 days

41
Q

why is it assumed the vascular changes could be playing an active role rather than passive in CSD?

A
  • arteriolar dilation propagates ahead of parenchymal changes of CSD
  • vascular cells release diffusible messengers (protein) that may influence activity of neighbouring neutrons and glial cells?
  • it is unclear whether whether electrical signalling or blood vessel if involved changes first?
  • could be that majority of changes are in the blood vessel first and then have an affect on nerves
42
Q

how is the trigeminal nerve involved in the pathophysiology or modulation of attack in migraine?

A
  1. Trigeminal (TG) nociceptive afferents innervate pain sensitive structures ,
    including vessels, meninges and pericranial muscles and fascials.
  2. Activation of TG nociceptive terminals stimulates release of neuropeptides (e.g. CGRP)
    which can increase the sensitivity of perivascular nociceptors and dilate cranial vessels.
  3. Central TG neurons terminate at the trigeninocervical complex (TCC) and CGRP release here can facilitate nociceptive trigeminovascular input.
  4. Plastic changes at the TG and TCC result in both peripherally and central activation and is thought to play roles in development of headache and allodynia causes by sensitisation.
  5. TCC is modulated by ascending and descending pain modulating systems at the cortical and subcortical level.
43
Q

why is migraine considered as multi-symptom complex event?

A

because it does involve one region or pathways rather is product of multiple regions and pathways being disrupted

  1. cortical - visual, sensory, cognitive, motor symptoms
  2. hypothalamic activation (yawning, polyuria, fatigue,mood change)
  3. brainstem activation - nausea, vomitting, dizziness/vertigo
44
Q

what is the potential functional role of CGRP in cerebrovascular regulation

A
  • CGRP is a neuropeptide involved in the transmission of pain
  • clinical trials have found CGRP drugs could be effective in migraine
  • The cerebrovascular trigeminal neuronal system, in which CGRP is the most potent vasoactive constituent, may participate in a reflex or local response to excessive cerebral vasoconstriction that restores normal vascular diameter.
45
Q

what is the role of BBB in migraine?

A
  • Detection of the prevalence of white matter hyperintensities in migraine patients determines its correlation with migraine severity, type and duration.
  • Negm et al. (2018) an MRI study in 2018 White matter hyperintensities are present in 43.1% of migraine patients. Age, presence of aura, nausea, disability during attack, resistance to treatment, and severity of headache and duration of migraine are considered a risk factor for development of white matter hyperintensities
46
Q

what mechanism transforms migraine into chronic migraine?

A
  • mechanism that transform migraine into chronic migraine are not fully understood but theories include:
    1. Atypical pain processing
  • failure to regulate descending pathways modulating pain processing e.g. cutaneous allodynia
  • recurrent migraine attacks leads to central sensitization
  • cortical hyperexcitability
    2. Atypical processing in other brain regions (apart from cortex)
  • sensory, affective and cognitive pain processing
    3. Neurogenic inflammation
  • excessive release of vasoactive peptides such as CGRP
  • excessive levels in CM compared to EM, could either be a consequence or cause
47
Q

how does the medication overuse cause headache?

A
  • leads to increased excitability of cortical and TG neurones
  • may facilitate CSD and trigeminal sensitisation
  • underlying mechanisms could be due to central NT dysfunction affecting nociceptive modulating system and other vegetative functions in patients w primary headache
48
Q

what is medication overuse headache (MOH?

A
  • MOH also known as rebound headache: occurs when analgesics (codeine, barbiturates) taken frequently to relieve headaches
  • have the propensity to aggravate headache frequency and induce refractory state daily or nearly daily-headache
  • not a separate headache entity but a reaction of migraine patients to a particular medicine
  • by stoping taking analgesics: hproptotion of patients substantial improvement in severity and frequency
  • however, even after cessation of analgesics, many patients continue to have headache, although might may feel clinically improved
49
Q

give an example of MOH

A
  • serotonin
  • low levels may increase CGRP activity in TG ganglion
  • low levels may increase expression of cortical receptors and increase CSD
50
Q

pituitary tumour

A

mostly benign

51
Q

epilepsy or headache, which of the two is a more common symptoms of brain tumour, provide evidence

A
  • Despite headache and seizures being the most common symptoms, a case control study using electronic primary care records in 2017 found that PPV of headache was 0.1% and seizure was 1.2%
  • risk of headache presented to primary care was less than 1 in 100
  • even when a secondary symptoms was present, the risk of brain tumour only rose to 4 in 1000
  • new onset seizure - overall risk of 1.2% rising to 2.3% if the patient was >60 years of age
  • suggesting isolated headache presented to primary care has too small risk of an underlying brain tumour and new onset seizure should be investigated further
52
Q

what are the symptomatic treatment for brain tumour?

A
  • intracranial malignancy requires both symptomatic and definitive treatments
    1. oedema (most high-grade malignancies) -> neurologic disability + raised ICP : corticosteroids- dexamethasone
  • dexmeth: 12-16mg/ day orally or IV
  • while they ameliorate symptoms, long term use has side effects: insomnia, obesity, diabetes mellitus
  • therefore, taper advised for administration
    2. seizures: anticonvulsant drug therapy (VPA, lamotrigine)
    3. venous thromboembolic disease: 20-30% o HGG and brain metastases - anti-coagulants used
53
Q

what is CDH?

A
  • not a diagnosis as it is not single entity rather includes a number of different headache includes: >4h daily: chronic headache chronic TTH, <4h daily: chronic closet headche, secondary: TBI, infections, iatrogenic, MOH
  • > 15 days
  • 4% of adults have daily or near-daily headaches (primary or secondary - essential to identify for management)
  • less common, 50% headache disorder in one year
54
Q

what is migraine and what are the symptoms associated?

A
  • episodic headache often accompanied by nausea and vomitting
  • associated w sensitivity: light, sound or movement
55
Q

what are trigger for headache/migraine?

A
  • brain of migraineur is sensitive to environmental and sensory stimuli
  • this sensitivity is ampler in women
  • amplified or initiated by trigger: glare, bright lights, sounds, other afferent stimulation; hunger; excess stress; physical exertion; stormy weather or barometric pressure changes; hormonal fluctuations during menses; lack of or excess sleep; and alcohol or other chemical stimulation.
  • knowledge of patients susceptibility to specific triggers is useful in management
56
Q

what are the treatment options for migraine ?

A
  • migraine can be modified and controlled by lifestyle adjustments, meds but it cannot be eradicated
    1. non-pharma:
  • identification and avoidance of specific headache triggers
  • good lifestyle: healthy diet, regular exercise, regular sleep patterns, avoid excess caffeine and alcohol, avoid acute changes in stress levels
  • reducing one’s stress by yoga, transcendental meditation, hypnoses, condition technique like biofeedback - for most, this is best as an adjunct to pharmacotherapy
    2. pharma: should be individualised, standard approach for all patients not possible
    a. anti-inflammatory (NSAIDs)
  • acetaminophen, aspirin, caffeine approved by FDA
  • side effects: GI dysfunction
  • general consensus: NSAIDs most effective when taken early
  • however, less than optimal in moderate or sever migraine
    b. serotonin receptor agonists (5HT1b/d),
    c. dopamine receptor antagonists
  • oral DRA as adjunctive therapy
  • drug absorption impaired in migraine due to reduced GI motility
  • therefore, when oral NSAIDs or triptan agents fail, addition of DA considered to enhance gastric absorption
    3. nasal spray
  • results in substantial blood levels within 30-60mins
  • in theory, they might provide faster and effective relief than oral but their reported efficacy is only approx. 50-60%
    4. other: narcotics
    5. preventative:
  • patient w increasing frequency of migraine attacks or that unresponsive or poorly responsive to abortive treatments are ideal for preventative treatments
  • NICE guidance: topiramate, propranolol (these 2 approved by FDA), acupuncture, riboflavin 400mg/day)
  • placebo controlled trails of onabotulinum toxin type A in episodic migraine negative but positive for chronic migraine
  • probability of success w any one of anti-migraine drugs is 50-70%
  • many managed w low dose propranolol, topiramate, gabapentin or VPA -> if these fail or unacceptable side effects -> second line agents: methysergide or phenelzine used
  • once stabilisation achieved -> drug continued for 6m -> tapered to assess the continued need
  • many patients able ti discontinue med and experience fewer and Midler attacks -> suggesting drug may alter natural history of migraine
    6. botox: blocks nerves - consider 3 monthly cranial Botox if poor response to 3 preventative drugs and MOH adequately treated
  • ¾ respond to varying degree, ¼ no response
57
Q

what is migraine disability assessment score (MIDAS)?

A

it is well validated, easy to use tool used for assess the patients disease and disability

58
Q

what are the emerging treatments for migraine?

A
  1. CGRP modulation
  2. Neurostimulation
    - Occipital Nerve Stimulation: modulates thalamic processing in migraine
    - only promising approach rn: intractable disabling CDH management
    - also shown promise in chronic cluster headache, SUNCT/SUNA, hemicranial continua
    - Transcranial Magnetic Stimulation
    - Vagal Nerve Stimulation
59
Q

what are the symptoms tension type headache and its treatment?

A
  • chronic head pain characterised w bilateral tight, bandlike discomfort
  • analgesics: acetamophin, aspirin or NSAIDs
  • triptans: effective in TTH when migraine present
  • amitriptyline: only proven treatment for chronic TT
  • tricyclics, SSRIs, benzodiazepine shown not effective
  • no evidence for efficacy for acupuncture
  • placebo controlled trails of onabotulinum toxin type A in chronic TTH also showed no benefit
60
Q

what is the management of CDH?

A
  1. preventative medication for CDH or TTH depending on the type
  2. intractable disabling CDH: difficult but only promising approach rn: occipital
61
Q

what is the management of MOH for out-patient and in-patients?

A

Outpatient
1. reduce dose by 10% every 1-2 weeks, immediate cessation for only patients w no contraindication
2. small doses NSAIDs (naproxen) if tolerated will relieve residual pain as analgesic is reduced
3. preventative medication introduced once the patients has substantially reduced analgesic use
- must be emphasised preventative generally do not work in the presence of analgesics
INPATIENTS: failed efforts at out outpatient withdrawal or have significant medical cognition such as diabetes mellitus -> hospitalisation for detoxification
1. analgesics withdrawn (completely on first day in absence of contradictions) + antiemetics and fluids administered
2. withdraws symptoms: clonidine e
- acute intolerable pain: aspirin
3. adequate hydration

MED627 (6 decks)

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