Secondary Headaches Flashcards
Analgesia-induced, TMJ dysfunction, Space occupying lesions, GCA [look at MSK], Raised ICP, SAH, Idiopathic Intracranial HTN, Trigeminal Neuroglia (32 cards)
Name Secondary headaches (8)
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’)
What is trigeminal neuralgia? Sx?
- 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
What is analgesia induced headache?
- 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
Dx of analgesia induced headache
- 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
Mx of analgesia induced headache
(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- Paracetamol + NSAIDs should be withdrawn abruptly
- Discuss with neurology if opioids are involved, and these will need to be withdrawn gradually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
Temporomandibular Joint Dysfunction: What is it? Causes? Signs? Tx?
(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
List some causes of Space Occupying lesions (5)
- Metastases
- Haematoma
- Hydrocephalus
- Cerebral abscess
- Meningitis
Presentation of Space Occupying lesions
(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)
Management of Space Occupying lesions
(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
What causes Subarachnoid haemorrhage (SAH)?
- 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.
Signs and Sx of SAH
(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
Ix for SAH (3)
(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
Mx of SAH (6)
(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
Rf for Idiopathic Intracranial HTN
(1. ) Obesity
(2. ) 3rd decade
(3. ) Drugs
(4. ) Endocrine abnormalities (Cushing’s, hypoparathyroidism)
(5. ) SLE
Presentation of Idiopathic Intracranial HTN
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
Ix of Idiopathic Intracranial HTN (5)
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
Mx of Idiopathic Intracranial HTN (4)
(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
Common Causes of Raised ICP
(1. ) Mass e.g. tumour, cysts, haematoma
(2. ) Oedema + infections e.g. meningitis
(3. ) Obstruction to flow e.g. hydrocephalus, impaired CSF absorption
Clinical features of raised ICP (5)
(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.
How may raised ICP cause herniation? What Sx are associated?
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
Mx of raised ICP
(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
How does increased ICP cause bradycardia?
(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
What is Extradural Haematoma? and how may it cause death
(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
What causes Extradural Haematoma? (4)
(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
