Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

neuro week 6 > ICL 10.1: Secondary Headache > Flashcards

ICL 10.1: Secondary Headache Flashcards

1
Q

what are the 2 secondary headache disorders?

A

these are headaches that are caused by something else!

  1. thunderclap headaches = SAH, RCVS, PRES, CVT, dissection
  2. stroke

honorable mentions = trigenminal neuralgia, pituitary apoplexy, spontaneous intracranial hypotension, giant cell arteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the SNOOP4 red flags of secondary headaches**

A

ⓢystemic symptoms and signs = fever, chills, night sweats, weight loss

Ⓝeurologic symptoms and signs = global or focal, AMS, unilateral weakness

Ønset sudden

Ønset at age older than 50 yo: very unusual for primary headache disorder to present after 50 yo

℗rogression of headache

℗recipitation of headache w/ valsalva: coughing, sneezing, bending over, heavy lifting indicate ICP

℗ostural headache = headache worse with standing

℗apilledema

℗regnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is a thunderclap headache?

A

acute, severe headache that reaches peak intensity at onset (that’s why it’s called a thunderclap headache!)

this is a neurologic emergency and urgent evaluation for secondary headache is recommended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what do you do if you think someone is having a thunderclap headache?

A

CT and if negative do a LP, possibly MRI, other neurovascular imaging

management and treatment depend on underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

45 yo woman presents to ED with intense global headache, which she experienced sudden onset of “the worst headache of my life”

Headache features: pancephalic, severe intensity

Asociated sx: photophobia, phonophobia, and neck stiffness

History of migraine

Family history: cerebral hemorrhage in mother

Exam: BP 180/100 mm Hg, no focal weakness

A

subarachnoid hemorrhage

“worst headache of my life” is like almost pathoneumonic for SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the clinical presentation for a thunderclap headache caused by a subarachnoid hemorrhage?

A

Worst Headache Of Life (WHOL): can be acute or several days to weeks

this is the most common cause of TCH (25% of TCH)

SAH carries poor overall outcome w/ significant morbidity and mortality, so initial eval of TCH should focus on ruling out SAH

associated features: nausea, vomiting, photophobia, neck stiffness, AMS, possibly HTN

causes: trauma > aneurysmal bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a sentinel headache?

A

a small aneurysmal bleed reported in 20 to 50% of TCH cases

so it’s a SAH but it’s not as big so you don’t pick it up as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what testing do you do if someone is having a SAH thunderclap headache?

A
  1. CT of the head without contrast

can be negative if the CT is done late in the game or it’s a small bleed (will be negative at 3 weeks)

  1. if that’s negative, do a LP to look for blood, a cell count and visual inspection for xanthochromia (yellowness from blood breakdown)
  2. mass spectrophotometry has 95% sensitivity at 12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you treat a SAH TCH?

A

Repairing source of bleed and preventing complications like lowering HTN to reduce headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when would you do an LP for a suspected SAH TCH and what would the results show?

A

you would do an LP if:
1. the patient presents with a first unusually severe headache

  1. TCH w/ negative CTH
  2. subacute progressive headache that is new and was a TCH at onset
  3. headache associated w/ fever, confusion, meningism, or seizures
  4. if you suspect high or low CSF pressure (even if papilledema is absent) if CTH does NOT show a mass lesion or other cause of symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

19 year old man comes to ED due to sudden onset of severe occipital headache, and in the waiting room he experiences first generalized tonic-clonic seizure

No past medical history, other than occasional migraines as a preteen

VS BP 165/95 mm Hg, Pulse 110 bpm, temp 99.3 degrees. He was lethargic and somewhat confused

Labs were remarkable for tox screen showing THC. He admits to daily pot smoking

A

reversible cerebral vasoconstrictive syndrome (RCVS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does RCVS stand for?

A

reversible cerebral vasoconstrictive syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is RCVS syndrome?

A

a type of TCH from cerebral vasoconstriction that is typically occipital though not necessarily

varies clinically w/ regard to presence and severity of neurologic deficits and imaging abnormalities

may present with focal deficits and/or seizures because this vasoconstriction can cause strokes, seizures, etc.

affects those 20 - 50 years of age ; women> men

described in peripartum period or in patients exposed to sympathomimetic drugs and SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what will imaging show for someone with RCVS?

A
  1. CSF normal
  2. imaging w/ diffuse, segmental, reversible cerebral vasoconstriction
  3. MRI brain with MRA head can show abnormalities but it can also be normal
  4. cerebral angiography is a gold standard for vessel imaging!! –> will show “string of beads” appearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do you treat RCVS?

A
  1. fluid bolus

2. calcium channel blockers like verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what things can cause RCVS?

A
  1. cannabis, cocaine, ecstasy, amphetamines, LSD, binge drinking
  2. sympathomimetics, nasal decongestants
  3. serotonergic drugs: SSRIs, triptans
  4. immunosuppressants: tacrolimus, cyclophosphamide
  5. nicotine patches
  6. herbal medications: ginseng
  7. blood products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which conditions predispose someone to developing RCVS?

A
  1. pregnancy
  2. eclampsia, preeclampsia
  3. neoplasia: pheochromocytoma, bronchial carcinoid, glomus tumour
  4. neurosurgery, head injury
  5. hypercalcaemia
  6. porphyria
  7. intracerebral hemorrhage, subarachnoid hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does PRES stand for?

A

posterior reversible encephalopathy syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is PRES?

A

a type of THC or severe acute headache that’s basically edema that’s reversible –> if it’s misdiagnosed or delay of diagnosis, it can cause infarct and permanent damage

patients will present with global and focal neurological signs and sx, AMS, visual loss, seizures

usually occurs with HTN crisis but can also be from eclampsia, specific drugs (immunosuppressants most commonly)

can occur in patients w/ RCVS initially, and vice versa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what imaging do you do for suspected PRES?

A
  1. CTH and LP are usually normal and often miss the diagnosis
  2. MRI however will show vasogenic edema most often in the posterior white matter and cortex, though frontal areas can be involved as well
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how do you treat PRES?

A

treat underlying cause which is usually HTN

or you might have to discontinue medication if someone’s on immunosuppressants or magnesium if someone was on it for eclampsia

22
Q

what is the prognosis of someone with PRES?

A

it’s favorable!

neurological status of most patients returns to baseline in days to weeks

23
Q

what is the cause of PRES?

A

the cause of PRES remains controversial, but the most popular theory is that severe hypertension causes interruption to brain autoregulation

cerebral blood flow is usually regulated by dilatation and constriction of vessels to maintain adequate tissue perfusion and to simultaneously avoid excessive intracerebral hypertension

breakdown in autoregulation occurs above a mean arterial blood pressure of 150 - 160 mmHg; in chronic hypertension, it occurs at higher pressures

so uncontrolled hypertension leads to hyperperfusion and cerebral vessel damage, resulting in interstitial extravasation of proteins and fluids, causing vasogenic edema

24
Q

31 yo woman comes to ED 48 hours after developing an instant sharp, shooting, severe pain behind the right eye for 5 minutes with nausea, photo, phonophobia. Since then, she has constant pain with fluctuating intensity in the right head, face, neck and shoulder

She has monthly migraine. These are unilateral (right or left), frontotemporal throbbing headaches associated with nausea, photo- and phonophobia

PMH: hypothyroidism, menstrual migraine, endometriosis

Medications include daily levothyroxine, oral contraceptives, and prn sumatriptan tabs (none recently)

Exam: normal except for fundus w/ mild BL papilledema

A

cerebral venous thrombosis (CVT)

25
Q

what does CVT stand for?

A

cerebral venous thrombosis

26
Q

what is a cerebral venous thrombosis?

A

it is the presence of a blood clot in the dural venous sinuses that usually causes a TCH

you can have a clot anywhere along the venous sinuses so in the superior sagittal sinus, straight sinus, sigmoid sinus, etc.

10% of CVT present w/ TCH w/o any other neurological signs or symptoms however most DO have neurological signs

27
Q

what is the clinical presentation of someone with a cerebral venous thrombosis?

A
  1. papilledema** (sign of increased ICP)
  2. seizures
  3. focal deficits

CVT headaches are persistent, progressive, exacerbated by Valsalva because of increased ICP

lying down increases ICP and can be painful

progressive obtundation where the distended cerebral veins will rupture into subarachnoid space

28
Q

what population is most often effected by cerebral venous thrombosis?

A

mean age of onset is 20 – 40 years

slight female preponderance, especially in young patients

29
Q

what causes cerebral venous thrombosis?

A
  1. idiopathic
  2. infection
  3. hemodynamic like dehydration, CHF, fever
  4. hypercoagulable states = pregnancy, factor V leiden,
  5. hormonal = oral contraceptives, pregnancy
  6. inflammation = SLE, sarcoidosis, IBD
30
Q

what imaging do you get for a suspected cerebral venous thrombosis?

A

MR venogram to see the blood flow through the venous system

31
Q

how do you treat a cerebral venous thrombosis?

A

depends on the cause

  1. anticoagulation/ thrombolytic therapy
  2. decrease ICP
  3. antibiotics, if septic CVT
  4. anti-epileptic medications
  5. surgery: thrombectomy, hematoma evacuation (rare)
32
Q

45 yo woman with sudden onset of left neck pain and left-sided headache while placing dishes on top shelf of cupboard

She came to ED for the following when she experienced transient left monocular blindness, and noted unequal pupils and left ptosis

PMH: migraine and hypertension

A

carotid dissection

carotid dissection is causing sympathetic chain damage which presents as Horner’s syndrome

33
Q

what are the risk factors for having a carotid dissection?

A
  1. HTP
  2. migraine

usually occurs in people over 50

34
Q

what are the symptoms of a carotid dissection?

A

can present with headache on side of dissection with or without neck pain can be the only manifestation of cervical artery dissection –> can present with TCH in isolation without associated signs of symptoms 20% of the time

headache is the most frequent symptom (55-100%), and the most frequent initial symptom (33-86% of cases)

associated signs : painful Horner’s syndrome, painful tinnitus, or painful hypoglossal nerve palsy

ischemia may occur in ipsilateral eye (transient of permanent blindness) or to brain depending on the progression of the dissection

35
Q

what imaging would you use for a suspected carotid dissection?

A

MRA or angiogram

looks like a flame sign from the acute tapering of blood flow

36
Q

how do you treat a carotid dissection?

A
  1. repair
  2. NSAIDs
  3. rarely anticoagulation
37
Q

what types of stroke present with headaches?

A

headache in 25% of ischemic strokes and 75% hemorrhagic strokes!!

CTH diagnostic in hemorrhagic stroke

but CT will be normal in recent, small, or posterior circulation ischemic stroke

38
Q

what conditions cause a thunderclap secondary headache?

A
  1. sucharachnoid hemorrhage
  2. RCVS = reversible cerebral vasoconstrictive syndrome
  3. PRES = posterior reversible encephalopathy syndrome
  4. CVT = cerebral venous thrombosis
  5. dissection (usually of the carotid)
39
Q

what is the clinical presentation of trigeminal neuralgia?

A
  1. severe, stabbing, lancinating, electric-shock like pain in the distribution of the trigeminal nerve
  2. attacks last from seconds to 2 minutes
  3. may be precipitated by mechanical factors such as wind, touch, toothbrushing, eating, drinking
  4. usually idiopathic irritation of trigeminal nerve, but do MRI to look for structural causes as well –> can be primary, or secondary to vascular causes, tumors, young people w/ BL sx- MS (2-4% of TGN)
40
Q

how do you treat trigeminal neuralgia?

A
  1. carbamazepine*
  2. gabapentin
  3. baclofen
  4. lamotrigine

you can do surgical options sometimes to burn the nerve or relieve compression but not common

41
Q

what is the ICHD-III criteria for trigeminal neuralgia?

A

at least 3 attacks of unilateral facial pain fulfilling the following:

  1. occurring in 1+ divisions of the trigeminal nerve with no radiation beyond the trigeminal nerve distribution
  2. pain has 3+ of the following characteristics: recurring in paroxysmal attacks lasting from a fraction of a second to 2 minutes, severe intensity, electric shock-like shooting, stabbing or sharp in quality, or precipitated by innocuous stimuli to the affected side of the face
  3. no clinically evident neurological deficit
42
Q

what is pituitary apoplexy?

A

acute, severe headache that can have a thunderclap onset due to acute hemorrhage or infarction of the pituitary gland

can be caused by pituitary adenomas, pregnancy, general anesthesia, bromocriptine therapy, or pituitary irradiation

43
Q

what is the clinical presentation of pituitary apoplexy?

A
  1. holocranial headache w/ an acute or thunderclap onset
  2. nausea, vomiting
  3. constriction of visual fields
  4. ophthalmoplegia
44
Q

how do you treat pituitary apoplexy?

A

surgical intervention

45
Q

what is spontaneous intracranial hypotension?

A

spontaneous CSF leak –> reduced ICP –> sagging of the brain –> traction on innervated meninges –> headache

can be caused by minor trauma, connective tissue disorder, or post epidural

46
Q

what are the symptoms of spontaneous intracranial hypotension?

A
  1. postural aggravation: better w/ lying down because increase of ICP, worse w/ getting up
  2. bilateral, neck stiffness
  3. auditory abnormalities or tinnitus, vertigo, diplopia
47
Q

what will you see on imaging of a patient with spontaneous intracranial hypotension?

A

CTH: low lying cerebellar tonsils

LP: low opening pressure

MRI w/ and w/o contrast, MRI spine: diffuse dural enhancement* and extradural fluid collections

Brain sag: low lying cerebellar tonsils, crowding of posterior fossa, subdural hematomas, effacement of prepontine cistern

CT Myelogram best for identifying site of leak

48
Q

how do you treat spontaneous intracranial hypotension?

A
  1. fluids
  2. caffeine

if those don’t help you can do a blood patch which is 20 mL of the patients own blood injected into the area of the leak

then if that fails, fibrin glucose injections

49
Q

what is giant cell arteritis?

A

a headache syndrome caused by inflammation of blood vessels

most often seen in elderly females over 70 years old

high concern for amaurosis fugax which is a warning sign of permanent visual loss due to block of temporal artery flow (this is the end stage of GCA)

50
Q

what is the clinical presentation of giant cell arteritis?

A
  1. scalp tenderness
  2. jaw claudication
  3. polymyalgia rheymatica
  4. constitutional symptoms
51
Q

how do you treat giant cell arteritis?

A

high dose steroids

do a biopsy too

neuro week 6 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions