Peishieen Flashcards
State the features of tension type headache (6)
o No premonitory symptoms and aura
o Bilateral
o Constant, non-pulsatile tightness or pressure
o Mild/moderate intensity
o Gradual onset
o Not worse with activity but may improve with rest
State the features of migraine (6)
o May have premonitory symptoms and aura
o Unilateral or Bilateral
o Pulsating/ throbbing pain
o Moderate/severe intensity
o Worsened with, or caused by activity
o Presents with at least 1 other symptom (N/V or photophobia/phonophobia)
State the features of cluster headache (5)
o Unilateral (around the eye or along face)
o Variable pain
o Severe/ very severe intensity
o Causes restlessness or agitation when doing activities
o Presents with cranial autonomic symptoms on same side of headache (red, watery or swollen eye, nasal congestion/runny nose, sweating)
List the pharmacological agents that have demonstrated efficacy in the treatment of TTH (Acute vs Prophylaxis; 3 each)
o Acute
1) Paracetamol (alone or with caffeine)
2) Aspirin
3) NSAIDs: Ibuprofen, Naproxen, Diclofenac, Ketoprofen
o Prophylaxis
1) Amitriptyline (1st line) -> tricyclic antidepressant (TCA)
2) Mirtazapine (TCA)
3) Venlafaxine (SNRI)
What are the classification of tension type headahces?
o Infrequent episodic TTH: < 1 episode/month
o Frequent episodic TTH: 1-14 days/month
o Chronic TTH: 15 or more days/month
- More associated with Vitamin deficiencies
Describe the pathophysiology of migraine in relation to the various phases: premonitory, aura, headache, postdrome and interictal
o Prodrome
- Activation of the hypothalamus, as well as neuropeptides involved in homeostatic functions, may contribute to symptoms experienced during the prodrome phase (activation of the hypothalamus occurs prior to the onset of migraine pain)
o Aura
- Cortical spreading depression (CSD) is considered to be the primary pathophysiology behind the aura phase. CSD causes large wave of slow spreading depression in gray matter, inhibiting cortical activity -> causing changes to synaptic activity, extracellular ion concentrations, blood flow and metabolism + activate trigeminovascular system
o Headache (Ictal)
- Several neuropeptides (e.g CGRP) have been implicated in the sensitization of the central and peripheral trigeminovascular system, creating a state of hypersensitivity and contributing to both pain and non-pain symptoms during the headache phase.
o Postdrome
- There are a number of similarities in the symptoms experienced during the prodrome and postdrome phases. However, the precise pathophysiological events that underlie these symptoms remain uncertain.
o Interictal
- Some regions of the brain remain abnormally activated after headache cessation, including the olfactory regions, the midbrain, and the hypothalamus.
List the pharmacological agents that have established efficacy for acute (6) and preventive (3) treatment of migraine (and which are not established)
o Acute treatment
- NSAIDs ± other analgesics
- Triptans
- Ergotamine (Ergot Alkaloids; inferior to Triptan on outcome of headache relief at 2 hours)
- Opioids (not really established)
- Ditans (5-HT1F stimulator) and Gepants (CGRP receptor blocker; long term efficacy not determined)
o Preventive treatment
* Antiepileptics (e.g Topiramate, Valproate)
* Beta Blocker (e.g Propranolol, Metoprolol)
* Anti-CGRP antibody (Erenumab)
State the role of Triptans in migraine treatment
- Triptans are recommended for the acute treatment of migraine for patients for whom over the counter analgesics do not adequately relieve pain
- Most patients experienced pain relief within 2 hours
- Place in therapy:
o As a class, the triptans have largely replaced the ergot alkaloids, due to a better side effect profile
What are the contraindications of Sumatriptan? (8)
o Uncontrolled Arterial hypertension
o Coronary heart disease
o Raynaud’s disease -> spontaneous vessel constriction causing tissue necrosis
o History of ischaemic stroke
o Pregnancy and lactation
o Hypersensitivity to triptans,
o Concurrent administration with MAO inhibitors
o Myocardial infarct
Generally due to vasoconstrictive effects
State the potential targets for Anti-CGRP antibodies
Either target the CGRP protein (anti-CGRP), or the CGRP receptor (anti-CGRP receptor)
State what Erenumab targets
CGRP receptor
State the criteria in which a patient may be prescribed with Erenumab
Patients with episodic or chronic migraine who have not responded to at least 2 medical treatments, or who cannot use other preventative treatments because of comorbidities, side effects, or poor compliance
State the potential problem that may be caused by blocking CGRP activity
CGRP is a vasodilator.
CGRP might act as a ‘vasodilator safeguard’ during ischaemia therefore, mild and transient ischaemic events might be worsened in individuals who receive long term CGRP blockade treatment
State the ICHD-3 criteria for diagnosing Migraine without aura
At least 5 attacks that fulfil the following criteria:
* Headache attack duration: 4-72 hours (when untreated or unsuccessfully treated)
* Headache characteristics (≥ 2 of 4 characteristics)
o Unilateral location
o Pulsating quality
o Moderate to severe pain intensity
o Aggravation by or causing avoidance of routine physical activity (e.g walking or climbing stairs)
* At least 1 other symptom during headache
o N/V
o Photophobia and phonophobia
* Not better accounted for by another ICHD-3 diagnosis
State the ICHD-3 criteria for diagnosis of Migraine with aura
At least 2 attacks fulfilling the following criteria:
* Presence of fully reversible aura symptoms (at least 1)
o Visual
o Sensory
o Speech and/or language
o Motor
o Brainstem
o Retinal
* Characteristics (≥ 3 of 6)
o At least 1 aura symptom spreads gradually over ≥ 5 minutes
o 2 or more aura symptoms occur in succession
o Each individual aura symptom lasts 5-60 minutes
o Aura symptom (≥ 1 symptom) is unilateral
o Aura symptom (≥ 1 symptom) is positive
o Aura is accompanied or followed within 60 mins, by headache
AND not better accounted for by other ICHD-3 diagnosis
State the classifications of migraine and state what counts as MMD and MHD
o Episodic: < 15 MMD or MHDs
- In lifetime, must have experienced ≥ 5 migraine attacks lasting 4-72 hours
o Chronic: ≥ 15 MHD, of which ≥ 8 are MMD
- At least 3 months
o MMD = Monthly migraine days
≥ 2 migraine characteristics (see above)
If no aura, ≥ 1 symptom (see above)
o MHD = Monthly headache days
A day with migraine-type or tension type headache
What is the criteria for migraine prophylaxis to be considered?
- Generally based on the number of headache days per month and the degree of disability caused by the attacks (at least 2 days a month and some moderate disability caused to be considered)
See notes for exact days and severity of disability
Describe what is medication overuse headache
Diagnosis Criteria:
* Headache on ≥15 days/month in patient with pre-existing headache disorder
* Regular overuse of acute and/or prophylactic headache drugs for > 3 months
o Anything not simple analgesic/ NSAID or combi is at least 10 day/mth
o Anything that is simple analgesic/ NSAID at least 15 day/mth
* Headache cannot be better accounted for by another ICHD-3 diagnosis
What are non-pharmacological therapies for TTH? (7)
o Patient education and identify triggers (Headache diary)
o CBT (Cognitive Behavioural Therapy; decrease stress level and depressive symptoms), biofeedback, relaxation
o Physical and/or occupational therapy
o Lifestyle modification (include sleep hygiene)
What are red flags that may indicate secondary headache? (SNNOOP10)
1) Systemic symptoms including fever
* Potential infection
2) Neoplasm in history
* Pre-existing history of cancer; worried about brain metastases or oncological process causing more serious conditions that mimic headache
3) Neurologic deficit or dysfunction
* Unless inborn, should not have any form of asymmetry
4) Onset of headache is sudden or abrupt
5) Older age (over 50 years)
* Exposed to more chronic disorders; risk profiling may change over time
6) Pattern change or recent onset of headache
7) Positional headache
8) Precipitated by sneezing, coughing or exercise
9) Papilledema (swelling at back of eye)
10) Progressive headache with atypical presentation
11) Pregnancy or puerperium (post-partum)
12) Painful eye with autonomic features
13) Post-traumatic onset of headache
* May be underlying bleed or structural issues
14) Pathology of immune system such as HIV/ immunocompromised
15) Painkiller overuse or new drug at onset of headache (Medication overuse headache)
State how headache treatment efficacy is monitored and what is monitored (3)
o Headache diary
o Disability assessment (e.g. MIDAS)
- Objective way to measure disability before and after treatment
o Adverse effect from medications
DDI of Sumatriptan (3)
1) Monoamine Oxidase Inhibitor (MAOi)
● Concurrent administration of MAOIs and sumatriptan is CONTRAINDICATED
● Sumatriptan must not be used within 2 weeks of discontinuation of therapy with MAOIs
2) Ergotamine
● Concomitant use of ergotamine (eg Caffox, Cafergot) or derivatives of ergotamine (including methysergide, dihydroergotamine) is CONTRAINDICATED
● Avoid taking sumatriptan within 24 hours after taking these medications
3) Other Triptans or Triptan Combination Products
● Avoid taking different triptans or triptan combination products (e.g. zolmitriptan, naratriptan, etc.) within 24 hours after taking sumatriptan
Define acute symptomatic seizures, dissociative (non-epileptic) seizures and unprovoked seizures
Acute symptomatic seizure: Seizures that result from some immediately recognizable stimulus or cause, i.e. that occur in the presence or close timely association (about a week) with an acute brain insult (metabolic, toxic, structural, infectious, hypoxic, etc.)
Unprovoked seizure: Seizures occurring in the absence of a potentially responsible clinical condition (cryptogenic) or beyond the interval estimated for the occurrence of acute symptomatic seizures (remote symptomatic seizure)
Dissociative (non-epileptic) seizure: Abnormal paroxysmal psychic, sensory and/or motor manifestations which resemble (at least in part) epileptic seizures but are not related to abnormal epileptiform discharges -> no abnormal discharges = normal EEG
Define Psychogenic non-epileptic “seizures” (PNES)
o Partial alteration of level of consciousness with a partial preservation of awareness.
o Caused by stressful psychological experiences or emotional trauma
o Involuntary -> when stresses come, body reacts in this manner
Define epilepsy
Disease of the brain defined by any of the following conditions:
* At least two unprovoked seizures occurring > 24h apart
* One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
* Diagnosis of an epilepsy syndrome
Describe the underlying pathophysiology processes in seizures and epilepsy
o Hyperexcitability
- Occurs because there is an enhanced predisposition of a neuron to depolarize
o Hypersynchronisation
- Under abnormal circumstances, intrinsic reorganisation of local circuits lead to synchronisation and promotion of epileptiform activity generation.
State the clinical presentation of GTC seizures (6)
- Begins with stiffening of the limbs (tonic phase), followed by jerking of limbs and face (clonic phase)
- During tonic phase, breathing may decrease or cease altogether -> cyanosis of nail beds, lips & face; typically returns during clonic phase but may be irregular
- Limb stiffen such that it forms figure of 4 (see image below)
- Clonic phase usually lasts 1 minute, after which the brain is extremely hyperpolarised and insensitive to stimuli
- Incontinence may occur, along with biting of the tongue or inside of the mouth; breathing may be noisy and appear to be laboured
- Following the seizure, patient may have a headache and appear lethargic, confused or sleepy
State the clinical presentation of focal onset (with no dyscognitive features i.e no altered consciousness) seizures (4 types of symptoms)
Motor
- Clonic movements (e.g twitching or jerking) of the arm, shoulder, face, or leg
- Speech arrest (involve muscles of articulation; dysarthria)
Sensory
- Feelings of numbness or tingling
- Visual disturbances flashing lights
- Rising epigastric sensation
Autonomic
- Sweating, salivation, or pallor
- ↑BP, HR
Psychic (or somatosensory symptoms)
- Flashbacks, dé j à vu (memory
- Visual, auditory, auditory, gustatory or olfactory hallucinations
- Affective symptoms include fear (most common), depression, anger and irritability
Does normal EEG mean no epilepsy?
No
State the laboratory tests/investigations that may be used to diagnose Epilepsy (4) state their purpose and limitations if any
1) Scalp Electroencephalography (EEG)
* Essential tool for diagnosis and classification of seizures and epileptic syndromes
* If diagnosis of seizures or epilepsy is considered, epileptiform discharges on EEG confirm diagnosis
* A normal EEG DOES NOT exclude possibility of epilepsy
* Limitations:
o Not all Epileptic patients have an abnormal EEG
- 50% chance of showing epileptiform activity in a first awake EEG.
- 80-90% sensitivity with repeated awake sleep EEGs.
o EEG can be abnormal in normal persons
- False positive epileptiform discharges on EEG in asymptomatic adults: 0.5-1%
2) Video EEG
* Video recording concurrent with EEG -> can see outward manifestation and what’s going on inside the brain
* Cons:
o Can be expensive and labor intensive
o Its use typically limited to diagnostic problems that cannot be resolved easily in the routine EEG laboratory
3) Magnetic resonance imaging with gadolinium
* Ordered for: adult patient who presents with first seizure, especially for patients with focal neurologic deficits, suggestion of focal onset seizure
* To identify focal lesions (structural reasons for seizure episode)
4) Biochemical/toxicology (even if diagnosed with epilepsy, still need to run)
* Helps to rule out electrolyte abnormalities (contributory factors)
* Serum prolactin -> considerable variability, not used routinely
* Creatine kinase (CK) -> raised after GTC (violent contractions may cause muscle breakdown)
