Headaches - Part 2 Flashcards

1
Q

74 year old pt with 4 day Hx of headache
• Hx:
◦ Progressively worsening, intense character, no seizures, changes in consciousness
◦ Hard to open mouth/heat
◦ Hr 84 bpm, BP 134/81, temp 36.5
◦ Cranial nerve exam normal except reduced visual acuity in right eye
◦ Possible jaw claudication

Diagnosis?

A

• Dx: temporal arteritis
◦ Formation of immune inflammatory granulomas in medium sized arteries.
◦ Ophthalmological emergency
◦ Bloods: ESR and CRP
◦ Mx: high dose corticosteroids for 2 years
◦ Need temporal artery biopsy

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2
Q

42 year old female with hour long Hx of headache
• Hx
◦ Severe headache and nausea
◦ Hx of migraine attacks but this is different
◦ Felt as though someone punched her in back of head

Diagnosis?

A

◦ Subarachnoid haemorrhage
◦ Mx: urgent CT, LP to look for xantochromia
◦ Rx: nimodipine (CCP tha reduces spasm in rupture cerebral artery - preventing ischaemia) and bed rest
‣ If pt survives: cerebral angiography

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3
Q

32 year old man
• Hx:
◦ Worried he is having ‘mini-strokes’ like father
◦ Every few months: attacks where he sees shimmering light in corner of eyes and gets ringing in ears
◦ Occurs at end of day, lasting 1/2 hour
◦ Conscious throughout and never feels dazed/confused after

A

◦ Could be epilepsy: but not post octal phase
◦ Probably migraine aura without headache
◦ Rx: trial of antimigraine medication (sumatriptan)

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4
Q
  1. Question: main causes of subarachnoid haemorrhage
A
  • Rupture of arterial aneurysm: usually ‘berry’ at junction between arteries of circle of Willis (45%)
  • Trauma (45%)
  • AVM: rupture of haemangiomas, etc (10%)
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5
Q
  1. Question: What is your differential for intracranial tumours?
A

• Secondary brain tumours (metastatic): most common type of brain tumours in adults (90% of intracranial tumours)
◦ Sources: lung, kidney, breast, melanoma, and colon.
• Primary brain tumours:
◦ Axial or neuroepithelial tumours (~50%): brain matter itself
‣ Astrocytomas
‣ Oligodendrogliomas
‣ Medulloblastomas
◦ Extra-axial
‣ Meningioma (~15%). A slow-growing tumour of the meninges that compresses the brain (can usually be surgically removed with good prognosis)
‣ Vestibular schwannoma: may compress cranial nerve VIII (hearing loss) and VII facial palsy)
‣ Pituitary adenomas, prolactinomas, and craniopharyngiomas
◦ Other: choroid plexus papillomas, haemangiomas, pineal gland tumours, etc.

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6
Q

Question: at what level of spine should you insert a needle during and adult LP? What are the surface anatomy landmarks?

A

◦ The spinal cord in adults ends at L1/L2, with peripheral nerves extending beyond that as a loose bundle of nerve fibres floating in CSF but must be at or below L3/L4. This can be
◦ Landmark: tracing a line between the posterior superior iliac crests (Tuffier’s line), which marks the L4/L5 space.

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7
Q

What structures do you pass through as you perform an LP?

A
  • Skin
  • Subcutis
  • Supraspinous ligament
  • Interspinous ligament
  • Ligamentum flavum (first ‘give’ as you push the needle)
  • Dura mater (second ‘give’ as you push the needle)
  • Arachnoid space – the destination
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8
Q

What are the indications for doing an LP?

A
  • Diagnostic LP: looking for oligoclonal bands (e.g. multiple sclerosis), high protein (Guillain–Barré syndrome), blood or bilirubin (e.g. SAH), pathogens (e.g. bacterial meningitis, viral encephalitis), malignant cells (e.g. CNS lymphoma), or a rapid improvement in gait and cognitive function after removal of 30 mL of CSF (e.g. normal pressure hydrocephalus).
  • Therapeutic LP: intrathecal drug administration (e.g. haematological malignancy in children), temporary reduction in intracranial pressure (e.g. idiopathic intracranial hypertension
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9
Q

What are contraindications for an LP?

A

Raised intracranial pressure due to an SOL, as the sudden drop in pressure can cause the brainstem to cone through the foramen magnum. Suspect raised intracranial pressure in a history of early morn- ing headaches, nausea, and vomiting that are made worse by lying down or straining; in anyone with impaired consciousness, papilloedema on fundoscopy, focal neurological signs (e.g. nerve VI palsy). If there is any doubt about an SOL then imaging should be performed prior to LP.
• Increased bleeding tendency (e.g. patient on warfarin, disseminated intravascular coagulation).
• Infection at prospective site of puncture.
• Cardiorespiratory compromise. Deal with this before doing any other procedure.

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10
Q

What are the risks associated with doing an LP?

A
  • Headache. About 30% of patients will get a headache due to the intracranial hypotension. This risk can be minimized by keeping the patient lying flat for at least 2 hours. Some needle types are less likely to cause headaches then others (smaller calibre is better).
  • Nerve root pain. About 10% of patients will get pain in a lumbosacral nerve root distribution, due to irritation by the needle of one of the nerves that form the cauda equina. This can be minimized by inserting the needle slowly and withdrawing it from the cannula slowly. Provide analgesia and reassure the patient that the pain will gradually subside.
  • Infection at the site of the puncture
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11
Q

What are the main symptoms and signs of raised ICP?

A

• The main symptoms and signs of raised intracranial pressure are: Headache, often worse when lying down
◦ Nausea, usually first thing in the morning, after lying down all night Papilloedema, a swollen optic disc when visualized by fundoscopy Visual blurring
◦ Cushing’s reflex, a paradoxical bradycardia and raised blood pressure, often with irregular breathing Cushing’s peptic ulcer, causing epigastric pain

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12
Q

Name four reasons for raised ICP

A

◦ SOL, such as a tumour, haematoma, abscess, or cyst
◦ Cerebral oedema, secondary to trauma or some other lesion
◦ Increased blood pressure in the CNS, due to vasodilator drugs (glyceryl trinitrate (GTN) spray, Viagra), malignant hypertension, hypercapneic vasodilation, venous sinus thrombosis, or superior vena cava obstruction
◦ Increased volume of CSF (hydrocephalus), which can be due to obstruction of CSF drainage (e.g. by a tumour), dysfunction of the arachnoid granulations responsible for CSF reabsorption (e.g. SAH or meningitis irritating the granulations, idiopathic intracranial hypertension), or increased CSF production (by a choroid plexus papilloma)

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