Secondary Headaches Flashcards

Analgesia-induced, TMJ dysfunction, Space occupying lesions, GCA [look at MSK], Raised ICP, SAH, Idiopathic Intracranial HTN, Trigeminal Neuroglia

1
Q

Name Secondary headaches (8)

A

May be due to structural, infective, inflammatory or vascular conditions

(1. ) Analgesia induced headaches
(2. ) Space occupying lesions
(3. ) Intracranial bleeding
(4. ) Raised intracranial pressure e.g. tumour, idiopathic intracranial HTN
(5. ) Infection
(6. ) Inflammatory disease e.g. GCA
(7. ) Referred pain e.g TMJ dysfunction

(8.) Trigeminal neuralgia (not classed as ‘headache’)

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2
Q

What is trigeminal neuralgia? Sx?

A
  • Affects the face/jaw rather than head
  • At least three attacks unilateral facial pain in distributions of trigeminal nerves, with no radiations beyond this
  • Pain has at least three of the following four characteristics:
    (1. ) Reoccurring in paroxysmal attacks from a second to 2mins
    (2. ) Severe intensity
    (3. ) Electric shock like, shooting, stabbing or sharp
    (4. ) Precipitated by innocuous stimuli to the affected side of the face. Often - talking, eating, drinking, brushing teeth etc
  • No clinically evident neurological deficit
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3
Q

What is analgesia induced headache?

A
  • Overuse of acute pain relief (>2-3 times/week) for a previously diagnosed primary headache disorder (usually migraines and tension headaches)
  • Drugs that can cause these headaches include: Caffeine, Paracetamol, NSAIDs, Codeine, Triptans
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4
Q

Dx of analgesia induced headache

A
  • Headache occurring 10-15d per month in patients with primary headache disorder AND regular overuse of pain relief for >3m
  • Dull constant headache which is often worse in the mornings
  • As each dose of medication wears off, the pain comes back
  • The headache must not fit any other headache diagnosis better
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5
Q

Mx of analgesia induced headache

A

(1. ) Withdrawal of medication is the mainstay
- Paracetamol + NSAIDs should be withdrawn abruptly
- Discuss with neurology if opioids are involved, and these will need to be withdrawn gradually

(2. ) Medication should be avoided for at least a month
(3. ) Pt should be warned that Sx worsen at first, and improvements may not be seen for weeks

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6
Q

Temporomandibular Joint Dysfunction: What is it? Causes? Signs? Tx?

A

(1. ) Muscles + cartilage around TMJ joint become inflamed so the bones rub against each other
(2. ) Causes: Teeth grinding, wear and tear, arthritis, stress, uneven bite
(3. ) Pain around jaw, ear or temple, grinding noise when jaw is moved, difficulty fully opening the mouth, Jaw lock, headache around the temples
(4. ) Usually resolves itself, painkillers for headaches

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7
Q

List some causes of Space Occupying lesions (5)

A
  • Metastases
  • Haematoma
  • Hydrocephalus
  • Cerebral abscess
  • Meningitis
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8
Q

Presentation of Space Occupying lesions

A

(1. ) Brain tumour headache = worse in the morning and on bending or Valsalva manoeuvre
(2. ) N + V
(3. ) Change in mental status or behavioural change
(4. ) Weakness, ataxia, disturbance of gait
(5. ) Deficits of speech or vision
(6. ) Generalised convulsions (involuntary contraction of muscles)

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9
Q

Management of Space Occupying lesions

A

(1. ) Surgery
(2. ) Radiation or Chemo
(3. ) Mx of raised ICP
(4. ) Tx of other complications e.g. anticonvulsants for seizures
(5. ) Dexamethasone (steroids)
- For those waiting for surgery
- Dampen brain oedema and reduces inflammation and pressure

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10
Q

What causes Subarachnoid haemorrhage (SAH)?

A
  • Usually due to bleeding from a berry aneurysm in the Circle of Willis.
  • Can also be due to arterio-venous malformation, encephalitis, vasculitis, tumour, idiopathic.
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11
Q

Signs and Sx of SAH

A

(1. ) Thunderclap headache i.e. maximum severity within seconds, ‘Worse ever’. SAH until proven otherwise
(2. ) Neck stiffness due to meningeal irritations

(3. ) Focal Sx and signs
- May suggest site of aneurysm

(4.) Other Sx: Vomiting, Collapse, Seizure, Coma

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12
Q

Ix for SAH (3)

A

(1.) CT SCAN: detects 95% of SAH

(2. ) LP can be used if CT scan in -ve
- Test for xanthochromia (RBC broken down and makes clear CSF yellow)

(3. ) Cerebral angiogram
- Check for aneurysm anywhere so can be treated urgently

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13
Q

Mx of SAH (6)

A

(1. ) Resuscitation
(2. ) Nimodipine (Ca-antagonist) - reduces vasospasm to prevent ischaemia
(3. ) Pain relief = morphine, codeine, paracetamol
(4. ) Consider Antiemetics, Anti-convulsants = N+V? Seizures?
(5. ) Surgery: coiling/clipping
- early prevention to prevent re-bleeding
- procedure to repair the affected blood vessel and prevent the aneurysm from bursting again
(6. ) Monitor complications

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14
Q

Rf for Idiopathic Intracranial HTN

A

(1. ) Obesity
(2. ) 3rd decade
(3. ) Drugs
(4. ) Endocrine abnormalities (Cushing’s, hypoparathyroidism)
(5. ) SLE

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15
Q

Presentation of Idiopathic Intracranial HTN

A

Sx are caused by high CSF pressures

(1. ) Headaches
(2. ) Neck pain
(3. ) Pulsatile Tinnitus
(4. ) Blurred vision +/- diplopia
(5. ) CN6 palsy
(6. ) Other: fatigue, memory problems, low mood, anxiety

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16
Q

Ix of Idiopathic Intracranial HTN (5)

A

Important to rule out other causes to come to IIH Dx

(1. ) Assessment of eye: papilloedema
(2. ) Normal neurological examination
(3. ) Brain imaging must be normal
(4. ) Normal CSF content
(5. ) Elevated LP opening pressure

17
Q

Mx of Idiopathic Intracranial HTN (4)

A

(1) lifestyle: weight loss, diet
(2) drugs: acetazolamide, topiramate (AEDs), diuretics

(3) Consider CSF shunt or optic nerve sheath fenestration which reduces optic nerve swelling
- performed if vision is under threat

(4.) CSF drained to dec pressure

18
Q

Common Causes of Raised ICP

A

(1. ) Mass e.g. tumour, cysts, haematoma
(2. ) Oedema + infections e.g. meningitis
(3. ) Obstruction to flow e.g. hydrocephalus, impaired CSF absorption

19
Q

Clinical features of raised ICP (5)

A

(1. ) Headache worse on vaslvular movement, coughing, leaning forward
(2. ) Vomiting
(3. ) Neurological deficits e.g. seizure, impaired conscious level, changing in behaviour
(4. ) Vision Sx: Diplopia, CN6 palsy, papilledema
(5. ) Cushing’s triad = bradycardia, irregular respirations, widened pulse pressure.

20
Q

How may raised ICP cause herniation? What Sx are associated?

A

RICP causes by a mass lesions, haematomas etc can cause a brain shift. This displacement can take two forms:

(1. ) ‘temporal coning’ or uncal herniation
- Downward displacement of the medial temporal lobe (uncus) through the tentorium
- This may stretch 3rd +/- 6th CN = nerve palsy
- Causes pressure on cerebral peduncles = giving rise to ipsilateral UMN signs

(2. ) ‘tonsillar coning’ or cerebellar herniation
- Downward movement of cerebellar tonsils through the foramen magnum may compress the medulla
- Ataxia, CN6 palsy, upgoing plantar reflexes , loss of consciousness, irregular breathing, apnoea
- This may result in brainstem haemorrhage and/or CSF obstruction

(3.) As coning progresses, coma and death occurs unless the condition is rapidly treated

21
Q

Mx of raised ICP

A

(1. ) Primary Mx: Relieving the causes:
- Surgical decompensation of mass lesion
- Glucocorticoids to reduce vasogenic oedema
- Shunt procedure to relieve hydrocephalus

(2. ) Supportive Tx
- Maintenance of fluid balance + BP control
- Head elevation
- Diuretics such as mannitol

(3.) Intensive care may be needed

22
Q

How does increased ICP cause bradycardia?

A

(1. ) Elevated ICP restricts blood flow to brain, this decrease oxygen/tissue perfusion
(2. ) This signals to symp NS to inc HR and thus BP
(3. ) High BP is picked up by baroreceptor which decreases HR

23
Q

What is Extradural Haematoma? and how may it cause death

A

(1. ) Collection of blood between dura and skull but can occur in spinal column.
(2. ) Can lead to death via brain displacement/ herniation, raised ICP

24
Q

What causes Extradural Haematoma? (4)

A

(1. ) Fractured skull caused by severe head injury e.g. road traffic accident
(2. ) Often due damaged middle meningeal artery but may also follow a tear in dural venous sinuses.
(3. ) EDH in spinal column may follow the trauma of epidural anaesthesia or lumbar puncture

25
Q

Clinical features of Extradural Haematoma (8)

A

(1. ) May lose consciousness at the time of head injury +/- ‘lucid interval’ + deteriorate + lose consciousness again
(2. ) Severe headache.
(3. ) N+V
(4. ) Confusion.
(5. ) Weakness of an arm and/or a leg.
(6. ) Speech difficulties.
(7. ) Seizure

(8. ) Bradycardia +/- hypertension
- indicates raised ICP [Cushings triad: bradycardia, resp difficulty, wide pulse pressure)]

NOTE: EDH in the posterior fossa can produce a very rapid deterioration to death, measured in minutes

26
Q

Ix of Extradural Haematoma

A

CT scan

  • Good at detecting haematomas
  • It can also show any skull fracture that may be present
27
Q

Mx of Extradural Haematoma

A

Surgical Drainage

28
Q

What is Subdural haematoma? Causes?

A

(1.) A subdural haematoma (SDH) is a collection of clotting blood that forms in the subdural space. Can occur slowly.

(2. ) This may be:
- An acute SDH.
- A subacute SDH (this phase begins 3-7 days after the initial injury).
- A chronic SDH (this phase begins 2-3 weeks after the initial injury).

(3. ) Tearing of bridging veins occurs when veins are sheared during:
- rapid acceleration-deceleration of head.
- blunt head trauma
- but spontaneous SDH can arise as a consequence of clotting disorder, arteriovenous malformations/aneurysms or other conditions

29
Q

Presentation of Subdural haematoma

A

(1. ) Usually presents about 2-3w following trauma.
(2. ) The initial injury may be relatively trivial (or forgotten), particularly in an older patient on anticoagulants, or in the context of alcohol misuse.
(3. ) Sx tend to gradually progressive.
(4. ) Anorexia, N+V.
(5. ) Gradually evolving neurological deficit such as weakness, speech difficulties, increasing drowsiness/confusion or personality changes.

30
Q

Ex of Subdural haematoma

A

(1. ) Assess consciousness with Glasgow Coma Scale
(2. ) Check vital signs, look for bradycardia and HTN associated with raised ICP
(3. ) Neurological examination, including examination for pupil size and reactivity and papilloedema (which can indicate raised ICP).
(4. ) Look for evidence of external trauma to the head or elsewhere.

31
Q

Ix of Subdural haematoma

A

CT scan with contrast (subacute SDH) or without contrast (chronic SDH)

32
Q

Contraindications for LP

A
  • Signs and causes of RICP
  • coagulopathy
  • focal neurology
  • cardiovascular compromise (bradycardia and HTN)
  • infection at the site of LP
  • decreased GCS