Headaches Flashcards

1
Q

List primary headache disorders

A

1: Migraine 2: tension type headache 3: cluster headache and trigeminal autonomic cephalagias 4: other primary headaches

Can be considered as

  1. tension
  2. Traction
  3. inflammation
  4. vascular process
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2
Q

Discuss pathophysiology of migraine

A

was thought to be vascular in origin however this has been disproved. Vascular changes are thought to be a epiphenomenon of what is an underlying primarily neurological event Abnormal tirgeminal nerve activation possibly triggered by cortical spreading depression leads to pain and sensitization of higher order neurons in the brainstem and thalamus

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3
Q

Discuss retinal migraines

A

rare syndrome consisting of recurrent attacks of monocular visual dysfucntion and may include positive features such as scintillations or negative features such as blindness. As with all migraines is completely reversible

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4
Q

Discuss hemiplegic migraine

A

characterized by a motor aura include hemiplegia and hemiparesis. Neurological symptoms can last up to 60 minutes followed by a headache. Rarely the motor deficit is persistent a consequence of a true migrainous stroke

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5
Q

Discuss brainstem migraine

A

common neurolgoical finding include dysarthria, tinnitus, vertigo, diplopia and ALOC

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6
Q

List triggers for migraine headaches

A

sleep deprivation stress hunger hormonal changes including menstruation OCP nitroglycerin

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7
Q

Discuss abortive therapies for migraines

A

For mild to moderate attacks simple analgesics are often effective. Gastric stasis is often present in true migraines and may limit the effectiveness of oral agents. Prokinetics such as metoclopramide may aid in absorption and make treatment more effective. Dopamine antagonists such as prochlorperazine, metoclorpamide and droperidol are highly effective as a monotherapy for acute migraine attacks. Sumatriptan is a selective 5ht agonist and can be effective in treating headache. Common side effects of triptans include chest pain, throat tightness, flushing. Do not use in pregnancy, htn, CAD Can use dexamethasone 10mg to reduce re-presentation of migrainous patients

Sphenopalitine blocks can be useful for the treatment of acute migrainous headache. 1ml of 1% lidocaine areoroslized using an atomizer .

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8
Q

Discuss cluster headaches

A

Cluster headache is the only headache syndrome that is more common in men then in women. Headache tend to occur repeatedly during a specific period of time interval. Several precipitating factors have been identified include the ingestion of alcohol, stress and climate change. As with migraine abnormal activation of the trigeminal nerve contributes to headache nocioception. Secondary parasympathetic activation causes typical associated symptoms such as rhinorrhea and lacrimation.

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9
Q

Discus clinical features of cluster headache

A

Occur suddenly with little warning. Multiple episodes often occur in a 24 hour period. Episodes can last from 15minutes to 3 hours Pain is typically unilateral stabbing pain to the eye which may awaken patient from sleep. Symptoms occur specifically in a trigeminal distribution Patient present agitated, ancious rocking rubbing the head and pacing. Attucks often subside rapidly leaving the patient exhausted. Can have ipsilateral autonomic symptoms such as ptosis, miosis and forehead or facial sweating.

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10
Q

Discuss DDX of cluster headaches

A

Carotid artery dissection which should be excluded in patients who present with unilateral face or neck pain and Horners syndrome. Trigeminal neurolgia – pain peaks within seconds and usually only last a few minutes. rare trigeminal autonomic cephalagias

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11
Q

Discuss management of cluster headaches

A

High flow oxygen is first line– delievered through a non rebreather at a rate of 12 L/min it aborts the headache within 15 minutes in 80% of patients. Subcut sumatriptan can be tiralled. Once presenting headache has been managed need to try to reduce further headache – use of prednisone 100mg for 5 days with a 12 day taper is recommened. Verapamil can be consided 120mg TDS

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12
Q

Discuss tension headache

A

Most common recurrent headache disorder but a rare cause for ED presentation. Women are affected slightly more then men. By definition episodic tension type headache can last as little as 30 minutes and as long as 7 days. PAtients typicall present with a tight bandline discomfort around the head that is nonpulsating and dull.

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13
Q

Discuss subarachnoid haemorrhage

A

80% of patient with nontraumatic SAH have a ruptured saccular aneurysms. Other causes include AVMs, cavernous angiomas, mycotic aneuroysms, neopalsms and blood dyscrasias. Most cases of SAH occur between the ages of 40-60 80% of patient will have a thunderclap headache described as the worst headache of my life. 20% of patient will have onset with exertion, valsalva or sex Peaks within seocnds to minutes – associated features include syncope, neck-stiffness, nausea and vomiting, photophobia and seizures. Signs depend on the extent of the SAH. Meningismus is present in more than 50% of patients and up to 20 % have neurology. 3-rd or 6th nerve palsy can be present. Up to 30% of patient recall a sentinel headache several days earlier

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14
Q

Discuss the Hunt and Hess scale of subarachnoid haemorrhage

A

stratifies patients according to their clinical signs and symtpoms patients with grade 1 or grade 2 haemorrhage have good prognosis those with grade 4-5 tend to do poorly - mortality

Grade 0 - unrurpauted aneurysm wihtout symptoms 0% mortality

Grade 1- asymptomatic or minimal heache with slight nuchal rigidity - 1-3%

Grade 1 a- no acute menigneal or brain reaction but with fixed neuro deficit 1-3%

Grade 2- Moderate to severe headache nucahl rigidity no neurlgoical deficit other than CN palsy 3-55

Grade 3- drowsy confused or mild deficit 9-19%

Grade 4 Stupor moderate to severe hemiparesis, possible early decorticate rigidity and vegetative disrubtances 23-42%

Grade 5- deep coma decerebrate rigidity moribund 70-77%

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15
Q

List a DDX for SAH headache

A

carotid artery dissection, cerebral venous thrombosis, reversible cerebral vasoconstriction syndrome, haemorrhagic or ischaemic stroke and primary headache disorders.

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16
Q

Discuss diagnostic testing of SAH

A

CT scan urgently sensitivity is for SAH is greater then 90% however this reduces to les then 50% by the end of the first week.

There is one well designed study taht showed 100% sensitiviyt and specificity for CT if performed within 6 hours time.

Current guidlines are still to perform LP for xanthochromia if suspected.

To differentiate a traumatic LP from a SAH the patients CSF is spun and the supernatant observed for xanthochromia. This yellowish pigmentation is secondary to the metabolism of HB a proces that can take up to 12 hours to occur.

If diagnosis is confirmed a CTA should be ordered – this is a reasonable first line in low risk patient, those who refuse LP who are still reasonable high risk for SAH,.

Up to 90% of patients with SAH have a cardiac arrhythmia or ECG abnormalities suggestive of acute cardiac ishcaemia. Typical finding include ST-T wave chagnes, u waves and QT prolongation

17
Q

Discuss management of SAH

A

Primary goals a aimed at treating acute medical and neurological complications, preventing recurrent ahemorrhage and forestalling ischaemic complications of vasospasm.

As grade 3 SAH and higher are at risk of resp failure and hypercapnia which can worsen ICP early intubation is often necessary for these patients.

PREVENTION OF DELAYED CEREBRAL ISCHAEMIA: Nimodipine should be started as soon as possible post diagnosis to prevent spasm. Oral dosage is 60mg by mouth or NG every 4 hours. Should have HD monitoring at this stage. Antifibrinolytics (aminocaproic acid) is used to reduce the risk fo early rebleeding

Bp management is determined by patient clinical status, in general a BP less then 160 and a MAP less then 130mmhg unless vasospastic.

Use labetalol or hydralzine. Vasodilators such as snip or GTN should be avoided due to a propensity to cause increase cerebral blood volume and increase ICP.

18
Q

Discuss Giant Cell Arteritis

A

inflammatory vasculopathy that occurs in medium and large arteries. Typically involves the large branches of the aorta and has a predilection for the extracranial branches of the carotid (temporal and occipital)

Mean age of onset is 71 year old and is rare before 50

Women are more commonly affected then men. In the majority of cases loss of vision is due to arteritic anterior ischemic optic neuropathy.

Headache is the most common initial features and occurs in more then 70% of patients. Headache is often 2-3 months in duration and can be intermittent. Usually is localised to the temporal region. Jaw claudication secondary to vascular insufficiency of the masseter and temporalis muscles.

Sysetmic features are often present including fever, anorexia and weight loss. 40% of patient develop syhmtpoms of polymyalgia rheumatica

The most serious complication of GCA is permenant vision loss amaruosis fugax can occur before permanent vision loss.

Signs including tenderness or reduced or absent pulses to the temporal artery with erythema and nodularity or swelling. VA, fields and fundoscopy should be performed. The presence of relative afferent pupillary defect should icnrease the suspcifion of GCA.

19
Q

Discuss diagnosis and mangement of GCA

A

Majority of patient will have a significantly raised ESR usually to more than 50mm/hr and often more than 100mm/hr as well as raised CRP, thrombocytosis and anaemia. Relatively poor specficity and sensititvity however only 4% of patient with GCA will have a normal ESR and CRP.

Can consider doppler US of the temporal arteries revealing a peri-luminal hypoechoic halo

The only test that confirms a diagnosis of GCS is a temporal artery bopsy

Those with amaurosis fugax or diplopia with TA need to start urgent glucocorticoids as they are at risk of permanent visual loss. Those with visual symptoms should have a methyl pred burst 100mg per day for 3 days.

20
Q

Discuss carotid and vertebral artery dissection

A

CAD causes approximatly 2% of strokes and in patient under 50 years of age is the most comon cause of ischaemic stroke.

May occur suddenly but is usually seen with an assocaited sudden neck movement or trauma. Reported mechanims invldue neck torsion, chiro, coughing heavy lifting interecourse or child birth.

The typical presentaiton of CAD is that of abrupt onset of pain in the head or neck often in association with symtpoms resulting from aischaemic consequences of the diessection and emboli. Neurology secodnary to cerebral ischaemia usually occur within the first few hours follwoign the onset of the headache or neck.

21
Q

Discuss carotid artery dissection

A

Classic triad is unilateral headache or neck pain sometimes radiating to the unilateral eye, ipsilateral parital horner’s syndrome and either blindness due to retinal ischaemi or contralateral motor deficits.

Acute severe retro-orbital pain in a previosuly healthy person with nil history of cluster is suggestive of carotid dissection.

22
Q

Discuss Discuss vertebral artery dissection

A

Less common then carotid dissection. Classic presnetation is that of a relatively young person with sever unilateral posterior headache and a rapidly progressive neurological deficit with sympomts of brainstem and cerebella ishcaemia.

Common finding including veritgo, severe vomiting, ataxia, diplopia, hemiparesis unilateral facial weakness and tinnitus.

23
Q

Discuss cerebral venous thrombosis

A

Thrombosis of the intracranial veins and sinuses is a rare disorder causing approximatly 1% of all strokes. Typically present with headache disproportionately affecting younger individuals

Mulitple causes and risk factors are classically linked to the Virchows triad. Both genetic and acquired prothrombotic conditions have been assoicated with CVT. Acquired causes include pregnancy and the puerperium, malignancy, head trauma, surgery, paramengieal infection and th OCP.

24
Q

Discuss clinical features of central venous thrombosis

A

Two major categories

1: those caused by increased ICP due to reduced venous drainage
2: those related to focal brain injury resulting in ischaemia infarction or haemorrhage

Diffuse headache increasing in severity over days to weeks is the most common symptom. Focal neurolgocial findings when present are related to the region of brain affected. Siezure both generalised and focal frequently occur. Occular finding including orbital pain, proptosis, chemosis extraocular msucle paralysis and papilloemea.

D-dimer can be used in those with low risk to exclude CVT

MRV is gold standard, CTV/A can be used in patient in whom an MRI is contraindicated or not available.

25
Q

Discuss idiopathic intarcranial hypertension

A

Relatively common seen in young obese women of childbearing age

The most prominent symptom is generalized headache which is goten gradual in onset and of moderate intensity. May wake patient from sleep and can be exacerbated by bending foward and the valsalva maneuver both of which impede CSF return.

Visual complaints are common and patients may experience transient visual obsucartion which are momentary blackouts of vision most likley due to tempoary disruption of the microscirculatory of the optic nerve.,

Papilloedema and VA and field deficit will be present in over 50% of pateint.

MRI/MRV is gold standard – if normal a lateral LP is performed with opening pressures.

26
Q

What are the crieteria for diagnosis of idiopathic intracranial hypertension.

A
  1. Headache that remits with normilization of CSF pressure
  2. Papilloedema
  3. nonfocal neurologic examination
  4. may have CN 6 palsy
  5. increased CSF oipening pressure
  6. Normal CSF studies
  7. Normal neuroimaging studies
  8. no other cause of ICP identified
27
Q

Discuss management of IIH

A

Removal of large amount of CSF >20mls is recommended in all treatment guidlines. CSF is produced relatively quickly and taps provide only short duration of relief.

For pateint with visual field loss rtreatment with medications to lwoer ICP is indicated. Acetazolamide is the most potent medication to lower ICP starting at 500mg BD

Other meds include frusemide,toperiamate, and steroids.

If not responsive to medical treatment referral to opthalmology for optic nerve sheath decompression or a neurosurgeon for CSF diversion procedure

28
Q

Discuss post dural puncture headache

A

Incidenc is highest in the 18-30 age group. Other risk factors include female, low BMI and history of chronic headache.

postulated to be due to persisant CSF leak outstripping production leading to CSF hypotenion. Cutting needles, larger bore and bevel not upright are at greater risk fr post dural headache.

Cardinal feature of pDPH is orthostatic or positional heacahe that is precipitate by the upright position. About 90% occur in the first 72 hours anjd typically resolve within a week.

Bed rest hydration and adequate hydration is adequate for most patients . Persistant headache methylxanthines such as caffiene and aminophylline have been used.

Epidural blood patch can be performed in severe refractory headaches.

29
Q

What is your DDX for thunderclap headache (8)

A
  1. Benign thunderclap headache
  2. Migraine
  3. Cluster
  4. SAH
  5. CAD
  6. CVT
  7. RCVS
  8. Pituitary apoplexy
30
Q

Discuss complications of SAH

A

EARLY

  • Rebleeding
    • Longer time to aneurysm treatment
    • worse neurological status on admission
    • larger aneurysm size
    • high systolic blood pressure
    • presence of intracerebral or intraventiruclar blood
    • acute hydrocephalus
  • Vasospasm and delayed cerebral ischaemia - tends to occur 3-15 days post headache with a peak incidence of 6-8 days
  • Eleavte ICP + hyodrocephalus
  • Hypnatraemia
    • occurs in 30% of SAH and is probably mediated by hypothalamic injury
    • SIADH - euvoloaemia
    • Cerebral salt wasting - hypovolaemic
  • Seizures
  • Anaemia
  • Cardiopulomary complications
    • Pulmonary oedema
    • Cardiac arryhtmia
    • ECG changes (ST depression, QT prolongation deep symmetric t-wave inversions and prominent u waves)
    • TNI rise can occur after SAH

LATE

  • Rebleeding
  • Anosmia
  • Epilipsy
31
Q

Discuss the ottowa subarach rule

A

For alert patients older than 15 years with new severe nontraumatic headache reaching a max intensity within 1 hour

Not for patients with

  • New neurological deficit
  • previous aneurysms
  • sah
  • brain tumors
  • history of recurrent headaches (>3episdoes over the course of >6months)

Investigation for SAH must continue if any of the following +ve

  • Age >40
  • Neck pain or stiffness
  • witnessed LOC
  • onset during exertion
  • thunderclap headache
  • limited neck flexion on exam
32
Q

Discuss Fisher Grade of SAH

A

Useful for predicting occurence and severity of cerebral vasospasms

  1. Grade 1
    1. no SAH or IVH detected
    2. Incidence of vasospasm 21%
  2. Grade 2
    1. Diffuse thin (<1mm) SAH
    2. No clots
    3. Incidence of vasospasm 25%
  3. Grade 3
    1. Localised clots and/or layers of blood >1mm of thickness
    2. No IVH
    3. incidence of symptomatic vasospasm 37%
  4. Grade 4
    1. Diffuse or no SAH
    2. ICH or IVH present
    3. INcidence of spasm 31%
33
Q

List diagnostic criteria for migraine wihtout aura

A

A) at least 5 attacks fulfilling criterai B-D

B) Headache lasting 4-72 hours (untreated)

C) headache has at least 2 of the following 4 characteristics

  1. Unilateral
  2. Pulsating quality
  3. Moderate or severe pain intesntiy
  4. Aggravation by or causing avoidence of routine activity

D) Druing headache at least one of the folowing

  1. Nausea and vomting
  2. Photophobia and phonophobia

E) not better accounted for by another ICHD-3 diagnosis

34
Q

Discuss diagnositic criteria for migraine with aura

A

A) at least two attacks fulfilling criteria B and C

B) One or moer of the following fully reversible aura symptoms

  1. Visual
  2. Sensory
  3. Speech and/or language
  4. Motor
  5. Brainstem
  6. Retinal

C) At least 2 of the following

  1. At least one aura symptoms spreads gradually over >5minutes and or two more symptoms occurs in successsion
  2. each indiviidual aura symptoms last 5-60 minutes
  3. at least one aura symptoms is unilateral
  4. the aura is accompanied or followed wihtin 60 minutes by headache

D) Not better accounted for by another ICHD-3 diagnosis and TIA has been excluded

35
Q

Discuss reversible cranial vasoconstrction syndrome

A

RCVS is a cerebral arteriopathy charactersied by segmetnal areas of vaso-constrction within large and medium sized vessels. It is the same disease as postpartum angiopathy or migraionous vasospasm.

Causes recurrent thunderclap headache in suceptible patients and may cause ischemic stroke or haemorrhage stroke.

36
Q

Describe polymyalgia rheumatica

A

An inflammatory rheumatic condition characterized by aching and morning stiffness about the shoulder hip girdle and neck

Bilateral shoulder pain is the presenting manifectsion in nearly all patients while neck and hip girdle are invovled in approxiamtly 70 and 50 percent resepctively.

Morning stiffness

Systemic signs

37
Q

Describe the World Federation of neurosurgens sub grading scheme

A

Grade 1 : GCS 15 with nil motor

Grade 2 GCS 13-14 with nil motor

Grade 3 GCS 13-14 with motor

Grade4 GCS 7-12 with motor

Grade 5 GCS >7