Headaches Flashcards

Question

Key difference between migrain and cluster headache?

Answer 1

Cluster - patient wants to keep moving, restless Migraine - wants to stay still in dark room

Answer 2

15-20% women 5% men

Answer 3

- Strong familial link - Triggers: chocolate, cheese, wine \* Query is whether the foods cause migraine or whether they are part of the craving as part of the prodrome \*

Answer 4

Wave of cortical spreading depression, decreased neuronal function

Answer 5

- Throbbing or pulsatile headache - Develops over minutes to hours - Light sensitivity, nausea and vomiting - Pain aggravated by movement - Prodrome: visual disturbance, sleepiness, food cravings, altered mood

Answer 6

Positive: zigzag lines, pins and needles Negative: blind spots, numbness

Answer 7

3+ of the following: - Pulsatile headache - 4-74hr duration - Unilateral - N&V - Disabling intensity - FHx

Answer 8

\>15 days/month for 3 months

Answer 9

Any red flags Status migrainosus Treatment in primary care not working \*\*important to consider medication overuse headaches first \*\*

Answer 10

Clinical diagnosis MRI + lumbar puncture needed if: - \>50yrs and new headache - Fever - Thunderclap headache - Neurological deficit - New congitive dysfunction - Drowsiness - Change from normal headache - Compromised immune system

Answer 11

Lifestyle: Avoid triggers, stress management, sleep hygeine, hydration Address comorbidities: sleep apnoea, depression, anxiety Medication overuse: restrict medication to 2 days/ week COCP: stop if migraines with aura

Answer 12

1st: Simple analgesia: NSAIDs, paraceptamol, aspirin 2nd: Triptan ± NSAID e.g. sumitriptan - consider intranasal or subcut if patient vomits with migraines Do not offer opioids or ergots Review after 2-8 weeks

Answer 13

Consider if: impact on QoL and daily function e.g. 1+ per week, prologed despite treatment, acute treatment doesn't work Medication choice: daily propranolol, amitriptyline \*Consider treatment failed if highest dose of prophylaxis does not control migraines after 3 months - then refer to neurology

Answer 14

Frovitriptan on days migraine is expected Zolmitriptan

Answer 15

Attack lasting \>3 days

Answer 16

Typical presentation: bilateral pressing or tightening, non-pulsating pain - Mins-days - No nausea - Photophobia and phonphobia can occur - Pericranial tenderness 'A band of pain or pressure around the forehead with no neurological features'

Answer 17

- Affects up to 80% population - Rarely severe: most manage at home - Affects women and young more than men and older

Answer 18

- Cause poorly understood - stress, inappropriate eye prescription, contracted cranial muscles

Answer 19

Pain around forehead but no N&V or autonomic symptoms 3 types: 1. Infrequent episodic: \<1 day per month 2. Frequent episodic: 1-14 days per month for 3+ months (+ either photophobia OR phonophobia or neither but not both) 3. Chronic: 15+ days per month (+ either photophobia OR phonophobia or neither but not both) - patients with chronic TTH may also have N&V

Answer 20

Red flags? Refer to secondary care Episodic TTH: simple analgesia, identify comorbidities e.g. stress/ sleep disorders Chronic TTH: consider preventative treatment e.g. 10 sessions of accupuncture, low dose amitriptyline \*\*Be aware of medication-overuse headaches\*\* \*\*Do not offer opiods, if you think about offering opiods reconsider diagnosis\*\*

Answer 21

Tricyclic antidepressant - works as a SNRI

Answer 22

Agonists of 5-HT1B and 5HT1D receptors on blood vessels - causing vasoconstriction Reduces release of nociceptive neuropeptides e.g. substance P

Answer 23

Headache resulting in overuse of medication e.g. ergotamines, triptansopioids, NSAIDs, paracetamol - Headache should resolve after stopping medication - non-steroidals and paracetamol must be taken on 15+ days per month to be considered overuse - Opioids, triptans and ergotamine must be taken on 10+ days a month to be considered overuse

Answer 24

- Explain diagnosis and that withdrawal of over-used drug is mainstay of treatment - Consider whether drug can be stopped abruptly - Symptoms may get worse before getting better - Review after 4-8 weeks from withdrawing medication

Answer 25

- One of the trigeminal autonomic cephalgias - Referred to as suicidal headaches - Severe, unilateral periorbital pain associated with ipsilateral cranial autonomic symptoms e.g. conjunctival injection (red eye), lacrimation and eyelid oedema

Answer 26

15 per 100,000 Male predominance Increased prevalence in close family member

Answer 27

- Facial pain due to activation of opthalmic branch of trigeminal nerve - Autonomic symptoms due to activation of parasympathetic aspect of facial nerve \*Overall cause unknown\*

Answer 28

- Hallmark is timing: occur in clusters of daily headaches for weeks or months with periods of remission - Severe, unilateral, periorbital pain + eye symptoms - Pain: sharp, burning, pulsating, pressure - Attacks last 15-180 mins - Patient cannot lie still, agitated, pacing - Timing can often be predicted and triggers may be found e.g. alcohol, physical exertion

Answer 29

5+ attacks of severe-very severe unilateral orbital/ temporal pain lasting 15-180mins + at least one of: - Conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, eyelid oedema, forehead/ facial swelling/ flushing, meiosis/ ptosis, restlessness/ agitation Episodic: 80-90% cases, pain free for at least 1 month between attacks Chronic: 10-20% cases, 12months with remission periods \<1 month

Answer 30

- Exclude red flags Lifestyle: advise re triggers, adress sleep disorders, depression etc Acute: Sumitriptan/ zolmitriptan, 100% oxygen 12-15L through non-rebreathe mask (home oxygen can be provided) Refer: first clsuter headache (diagnosis is made by specialist), patients often have MRI scans done, if patients develop symptoms that may suggest secondary cause, if patient is pregnant Prevention: verapamil

Answer 31

AKA temporal arteritis because it most commony affects temporal artery - Systemic vasculitis that can cause blindness - inflammation in the walls of medium and large arteries - Uncommon - Causes a serious headache

Answer 32

5-18 per 100,000 over 55yrs - very uncommon in patients \<55 4x women than men

Answer 33

Granulomatous inflammation in walls of medium-large vessels especially superficial temporal artery - Vasculitic lesions consist of cellular infiltrate that forms giant cells - B cells direct antibodies to combat the vascular proteins causing inflammation in the vessels leading to narrowing and pain

Answer 34

- 75% have a headache - 60% have polymyalgia rheumatica (pain, stiffness and inflammation of muscles around neck and shoulders) - Fever - Scalp tenderness, overlying skin can be red - Loss of pulsation over temporal artery - Jaw claudication - Visual loss/ double vision

Answer 35

- FBC: low Hb, raised platelets - ESR and CRP are raised in most cases (a normal level does not exclude GCA) - Temporal artery biopsy needed for definitive diagnosis - shows intimal proliferation and narrowing of lumen + giant cells

Answer 36

SOCRATES - Headache red flags - Change in vision - Scalp pain/ tenderness e.g. when head on pillow or combing hair - Jaw/ tongue pain - Polymyalgia rheumatica questions e.g. trouble turning in bed or when lifting arms - Systemic: fever, night sweats, weight loss, anorexia - Arm pains: limb claudication - Chest pain

Answer 37

Low Hb (normocytic anaemia) + raised platelets

Answer 38

**Medical emergency - treat to prevent vision loss** - Initial management is glucocorticoids - high dose prednisolone - If patient has visual changes refer for urgen assessment by opthalmologists - they may advise giving pred in mean time - If no visual loss, refer via urgent GCA pathway for urgent assessment with rheumatology - Arrange for bloods

Answer 39

Used for cluster headaches only Causes vasoconstriction of intracranial blood vessels by acting on 5-HT1D receptors Used to be frequently used for migraine however this is no longer the case – known to cause medication overuse headache

Answer 40

- Managed in secondary care - Treatment 1-2yrs with glucocorticoids - To avoid glucocorticoid toxicity methotrexate or tocilizumab may be given - Patient reviewed every 2-8 weeks for 6 months, then every 12 weeks for 6 months then every 12-24 weeks for 12 months - Glucocorticoid dose tapered when patient in remission but relapse is common

Answer 41

This is defined as a return of symptoms regardless of whether inflammatory markers are raised - Visual disturbance: refer for urgent assessment - Be aware of the fact that GCA can affect aorta and proximal branches so look out for limb claudication, abdo pain, back pain

Answer 42

Known as high pressure headaches (normal ICP is 7-15mmHg) Pain occurs as excess CSF leads to stretching of meninges and activates pain-sensitive structures e.g. dura Symptoms: headache, vomiting, transient visual changes, increased on coughing or straining, worse lying down

Answer 43

- Mass effect: tumour - Brain ischaemia - Obstruction to CSF flow - Bleed - Infection - Idiopathic

Answer 44

Dull, generalised headache Worsened by anything that increases ICP e.g. coughing, lying down, sneezing, bening forwards Vomiting, papilloedema, visual changes

Answer 45

Pressure-volume relationship between ICP, volume of CSF, blood, brain tissue and cerebral perfusion pressure Cranial compartment is inelastic and the volume is fixed - The fluids create an equilibrium: increase in one of the fluids leads to a decrease in another Cerebral perfusion pressure = pressure of blood flowing to brain CPP = MAP - ICP (therefore raised ICP leads to less blood reaching brain)

Answer 46

- Treat the cause - Lumbar puncture, ventricular drain, shunt - If idiopathic: weight loss and acetazolamide

Answer 47

Berry aneurysms (think spider body)

Answer 48

- Most commonly due to head trauma or berry aneurysm - Peak incidence 50yrs - Thunderclap headache (worst they've ever had) - Photophobia, vomiting, loss of consciousness, deafness - Neck stiffness - Seizures - Patients report prodromal symptoms: a 'warning leak' transient diplopia, dueen severe headache

Answer 49

- HTN - Smoking - Family hx - Autosomal dominant PKD - Connective tissue disorders

Answer 50

95-90% in anterior circulation: mainly anterior communicating-ACA junction

Answer 51

**Emergency non-contrast CT: order thin slices to avoid missing small collections of blood** - sensitivity almost 100% within 6hrs of bleed - shows hyperdensity in subarachnoid space - Patients can be agitated and need anesthetising to be scanned U&E: hyponatremia occurs in 50% and is associated with vasospasm following SAH - Clotting profile - Blood glucose: hyperglycamia occurs in 1/3 - CT angio if CT negative but suspicion high

Answer 52

Yellowish discolouration of CSF occuring due to breakdown of RBCs following subarachnod haemorrhage \*This won't be apparent straight away as it takes time for RBCs to breakdown)

Answer 53

- ABC - Isotonic saline for fluid resus - As soon as diagnosis confirmed refer to neurosurgeons and give **nimodipine** (combats vasospams following SAH) - Observe closely - Consider seziure prophylaxis - Give stool softener and anti-emetic after surgery as any valsalva manouvre can cause increased ICP and re-bleed

Answer 54

- Surgical clipping: treatment of choice, mor invasive than coiling - Endovascular coiling: platnum coils placed into aneurysm, causes thrombotic occlusion (less invasive but higher risk of re-bleed)

Answer 55

Collection of blood following a bleed into the space between the dura and arachnoid mater

Answer 56

Bridging cortical veins that empty into the dural venous sinuses Bridging veins = veins that transverse the dura mater and empty into the dural venous sinuses (venous drainage of the brain)

Answer 57

Chronic and acute SDH are mainly caused by trauma - Seen in eldelry patients who have had a fall - age related brain atrophy causes veins to be more stretched and prone to bleeding

Answer 58

Usually due to shear forces disrupting bridging cortical veins - Bleeding causes intracranial pressure to rise, cerebral perfusion pressure and cerebral blood flow decreases - Ischaemic injury occurs

Answer 59

Seen in alcohol abusers (causes brain atrophy) or those who are taking anti-coagulants or have a coagulopathy Blood collects over \>21 days and becomes symptomatic when underlying brain tissue is compressed

Answer 60

Patients often have no trauma or present weeks after a fall/ trauma with vague symptoms of weakness/ confusion/ drowsiness

Answer 61

Acute: \<3 days old (diffusely hyperdense) Subacute: 3-21 days old (heterogenously hyperdense/isodense) Chronic: \>21 days (diffusely hypodense) Acute on chronic: areas of hypodensity + hyperdensity

Answer 62

- Recent trauma - Coagulopathy - Anticoagulant medication - 65+ - Chronic alcohol use

Answer 63

Risk factors, signs of trauma on face, lacerations/ bruising on head and neck, headache (due to raised ICP), unequal pupils size (anisocoria) (due to herniation), confusion, diminished verbal response

Answer 64

Bloods: coagulation profile, FBC Non-contrast CT Subdural fluid collection forms a crescent shape and may cause effacement of underlying sulci

Answer 65

Acute: reverse anti-coagulation, craniotomy and drainage of haematoma Chronic: can be left to spontaneoulsy recover if causing no problems, surgical manegement to remove blood either burr holes and then wash the blood out or craniotomy to remove the haematoma

Answer 66

Uncommon, caused by general tears with CSF leakage, trauma, lumbar puncture or spinal anaesthetic

Answer 67

Dull, throbbing headache made worse by standing and improved by lying down

Answer 68

Conservative: bed rest, increased fluid intake, caffeine (causes vasoconstriction) Epidural blood patch: blood from patient used to 'plug' hole in dura

Answer 69

Inflammation of the meninges \*\*\*Not inflammation of the brain tissue - this is encephalitis\*\*\*

Answer 70

Arachnoid and pia mater (aka the leptomeninges)

Answer 71

500mL, 350mL is reabsorbed into blood so we have 150mL of CSF circulating at any one time

Answer 72

Between pia and arachnoid mater (subarachnoid space) Normal to find a small amount of WBCs, proteins and glucose in the CSF Mainly lymphocytes in the CSF with very few polymorphonuclear WBCs (e.g. neutrophils)

Answer 73

- Autoimmune disease e.g. lupus - Reaction to medication - Infection (the most common across all age groups)

Answer 74

- Direct spread: trauma or URTI allowing infection into CSF via the skull or spinal column - Haematogenous spread: pathogen enters blood and tracks to CSF

Answer 75

Epidemics (18-50yrs): n.meningitidis (meningococcus meningitis) Head trauma: strep.pneumoniae Immunocompromised: L.monocytogenes \<3 months: group B strep 3 months-18yrs: n.meningitidis \>50yrs: strep.pneumoniae

Answer 76

Bacterial - Requires early and aggressive treatment

Answer 77

4/100,000 in UK per year Peaks: infants and adolescents

Answer 78

**Pneumococcal:** protection against serious infections caused by pneumococcal bacteria, including meningitis **Hib/ Men C:** protection against a type of bacteria called meningococcal group C bacteria, which can cause meningitis **Meningitis ACWY:** given to freshers, protection against 4 types of bacteria that can cause meningitis: meningococcal groups A, C, W and Y.

Answer 79

H.influenzae, strep.pneumoniae, n.meningitidis all colonise nasal and skull cavities - Immunodeficiency or breach of structural defence allows bacteria into intracranial compartments - Overtime inflammatory response occurs and polymorphonuclear cells enter CSF - The inflammation leads to the symptoms of meningitis

Answer 80

\>5 WBCs in 1uL of CSF usually indicates meningitis - The amount of WBCs in CSF indicates which type of infection is causing the meningitis: **Bacterial meningitis CSF:** - 1000s WBCs (mainly polymorphonuclear e.g. neutrophils) - Very high opening pressure, very high protein, high lactate, \<50% CSF:serum glucose ratio (bacteria use the glucose so it decreases in the CSF) **Viral meningitis CSF:** - 100s WBCs (mainly mononuclear) - Mildly increased opening pressure, mildy raised protein, \>50% CSF:serum glucose, normal lactate

Answer 81

Very high opening pressure (\>25cm H₂O) 1000s of polymorphonuclear WBCs High lactate Very high protein levels

Answer 82

Pressure of CSF detected just after needle placed in spainal canal Indicates intracranial pressure

Answer 83

Presence of large numbers of WBCs - causes pressure increase

Answer 84

- Fever - Meningism triad (neck stiffness, photophobia, headache) - Purpuric, non-blanching rash: suggests meningococcal septicaemia **(the rash occurs because a systemic inflammatory response occurs and causes disseminated intravascular coagulopathy which causes vasodilation, capillary leakage and haemorrhaging into skin)** - Neurological complications: - increased ICP headache, N&V - Seizures (20%) - Focal neuro deficits (10%)

Answer 85

Infections caused by the bacteria n.meningitidis Most commonly causes: - Meningococcal meningitis - Meningococcal septicaemia

Answer 86

Clinical hx, presentation and examination form initial diagnostic approach - If bacterial meningitis is suspected, immediately commence antibiotics - Definitive diagnosis made when microbial organism is found in CSF

Answer 87

Signs of raised ICP: GCS score \<13, focal neurological signs, abnormal posturing, following seizure if not stable, dolls eye movements - **this is because it could cause a drop in ICP and herniation** If rash suspicious of meningococcal septicaemia - you don't want to introduce the infection into the CNS Bradycardia w/ HTN, immunocompromised, systemic shock, coagulopathy, respiratory failure

Answer 88

Bloods: CRP, PCR of blood to identify causative organism Lumbar puncture (unless contraindicated) CSF: electrophoresis showing presence of oligoclonal bands (bands of immunoglobulins seen when analysing CSF) - presence of these in the CSF indicates CNS inflammation Kernig's sign: patient lies on back, flexes hip to 90^o - leg straightened at knee causes back pain - pain occurs as lowering of leg stretches meninges and if they are inflamed it exacerbates pain

Answer 89

**Bottom line: don't wait to give antibiotics if you suspect bacterial meningitis** If suspecting bacterial meningitis + non-blanching rah: give IV/ IM **benzylpenicillin** asap in part of limb that is still warm If suspecting bacterial meningitis without non-blanching rash don't give antibiotics unless patient will not reach hopsital urgently

Answer 90

**If suspecting bacterial meningitis, give broad spectrum antibiotics immediately - don't wait for results of investigations** - Usually a 3rd generation cephalosporin **ceftriaxone** - Once species identified antibiotics adjusted - IV antibiotics for minimum of 2 weeks

Answer 91

Acyclovir if suspecting encephalitis Steroids if CSF evidently infected e.g. purulent/ high WBCs Treat precipitating factor e.g. trauma Supportive treatment for shock and raised ICP Complication management e.g. drain abscess

Answer 92

Consult regional health protection unit - Identify contacts who are at raisk and prescribe/ supply prophylactic treatment \*\*Bacterial meningitis and meningococcal disease are notifiable diseases

Answer 93

Viral Usually self-limiting and patients recover without major neurological complications

Answer 94

3000 cases reported each year but true incidence thought to be much higher

Answer 95

Coxsackievirus B, herpes simples type II \*\*In most cases no organism is found\*\*

Answer 96

Virus enters through skin lesion, GI, respiratory or urinogenital tract and then replicated locally It then enters CNS via blood stream or by tracking along cranial/ peripheral nerve

Answer 97

Similar presentation to bacterial meningitis but less severe - Seizures, focal neurological deficits Profound changes in consciousness are rare in viral meningitis (if present, suspect encephalitis)

Answer 98

- Difficult to culture viruses from CSF - Often a clinical diagnosis as difficult to identify organism - Viral meningitis can be distinguished from bacterial via CSF analysis (viral = lower WBCs in 100s, normal lactate, mild protein increase)

Answer 99

- Benign, self limiting condition - If a headache perists + visual impairment there may be impaired CSF reabsorption following inflammation - this can lead to raised ICP - CSF diversion procedures can be carried out to relieve the ICP

Answer 100

Inflammation of the neuronal and glial substance of the brain (the brain parenchyma) - Can be caused by infectious agents or by an autoimmune process

Answer 101

HSV1 - early treatment with aciclovir reduces from 70% to 20-30%

Answer 102

1 in 100,000 annually

Answer 103

Most commonly identified cause is HSV1 - \>90% cases Immunocompromised patients: CMV, HIV, JC viruses

Answer 104

- Organism enters body via inhalation/ other - Gains access to CNA via olfactory mucosa and cranial nerves leading to diffuse inflammation in basal frontal and medial temporal lobes

Answer 105

- Headache, fever, seizures, focal neurological deficits, significant mental status deterioration, photophobia, phonophobia, nuchal rigidity (neck stiffness) There may be a prodrome but HSV1 encephalitis often doesn't have a prodrome

Answer 106

Evidence of inflammation following CSF analysis + clinical ± radiological evidence of focal brain involvement CSF in viral encephalitis is similar to that of viral meningitis 90% patients have an abnormal brain MRI - findings depend on cause but often shows hyperdensity with T2/ FLAIR sequences

Answer 107

Without treatment HSV encephalitis has a high morbidity and mortality so most clinicians start acyclovir in patients presenting with features suggestive of encephalitis - IV acyclovir given for a minimum of 2 weeks - If caused by autoimmune condition, responds to IV steroids

Answer 108

Worst outcome with HSV1 - untreated has a 70% mortality and most patients are left with persistent neurological deficits

Answer 109

Swelling of caudal part of brain Characterised by headache, seizures, altered mental status and visual loss Imaging shows white matter vasogenic oedema affecting the occipital and posterior parietal lobes only Causes: HTN, kidney disease, infection, pre-eclampsia

Answer 110

The negative CT head does not exclude subarachnoid - they need a lumbar puncture **after 12hrs** to look for evidence of blood in the CSF

Answer 111

Gradient echo - MRI sequence Angiogram

Answer 112

3/10 people will experience this

Answer 113

Sensorineural hearing loss

Headaches Flashcards

(138 cards)