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Neurology > Central nervous system - secondary headaches > Flashcards

Central nervous system - secondary headaches Flashcards

1
Q

What is the clinical feature of Acute Glaucoma

A
  • Severe pain localized to the affected eye and may radiate to the ear, sinuses, teeth or forehead.
  • Blurriness, halos around lights and scotoma
  • Congenital narrowing of the anterior chamber angle that, under certain conditions, closes, resulting in a significant rises in intraocular pressure (IOCP)
  • Worsen when
    a) entering a low light
    environment,
    b) Mydriatics,
    c) sympathomimetic and
    d) anticholinergic
  • Examination
    i) Red eye
    ii) a fixed mid dilated pupil,
    iii) corneal clouding and
    iv) shallow anterior chamber

o Elevated IOP in the range of 60 to 90mmhg ( normally <21mmhg)

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2
Q

What are the treatment for acute Glaucoma

A
  • 1) B blockers - Timolol topical to eye BD
  • 2) Carbonic anhydrase inhibitiors - Acetazolamide 250mg
  • 3) Prostaglandlin F2 - Latanoprost .005% - 1 drop daily
  • 3) Osmotic agents
  • Prompt referral to ophthalmologist
  • Differential diagnosis – cluster headache, Acute iritis
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3
Q

What are the features of Brain Tumor

A
  • worsening headache that has been present for weeks to months
  • pain initially worse in the morning but became continuous
  • Pain is often bifrontal or bioccipital
  • Worsen by coughing, sneezing, bending, sexual intercourse
  • Often present to ED with seizure, personality changes, cognitive difficulties
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4
Q

Principle of disease ( Brain tumor)

A
  • headache is the most common complaint
  • commonly elderly
  • previous history of Neoplastic ( lung, breast, malignant melanoma, renal cancer, Gastric cancer)
  • primary tumors are rare typically occurs in < 50years of age
  • cause of pain is due to direct invasion or traction on pain sensitive structures
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5
Q

describe your treatment of Brain tumor

A
  • Urgent referral to neurosurgical
  • Dexamethasone – steroid if there is sign of increase of ICP
    (10mg IV – 4mg every 6hrs)
  • Anticonvulsant if present with seizure
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6
Q

What are the principle of Carotid and Vertebral dissection?

A
  • Most frequent cause of stroke in patient <45 years old ( 20%)
  • History associated with dissection include -:
    o Sudden neck movement
    o Trauma
    o Coughing
    o Minor fall
  • Pathological lesion – intramural hemorrhage within the media of the arterial wall. This can be local or spread circumferentially and occlude the vessel.
  • Distal embolization and platelet aggregation further complicate the condition.
  • Timing of the CNS symptoms can be days to years.
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7
Q

What is the clinical presentation for Carotid disection?

A

Classical triad -:
1) Unilateral headache – severe retro- orbital pain / throbbing headache with no history of cluster headache.
2) ipsilateral partial Horner’s syndrome < 50%
3) contra lateral hemispheric findings – aphasia, neglect, visual disturbance or hemi paresis
Warning symptoms – TIA, amaurosis fugax, syncope, episodic light headedness
- Factors associated with worse prognosis
o Old age
o Occlusive disease on angiography
o Stroke is the initial presentation

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8
Q

What is the clinical presentation for the Vertebral disection?

A
  • less common
  • relative young patient with severe unilateral posterior headache and neurological findings
  • symptoms rapidly developed i.e. cerebella and brain stem
    o vertigo
    o severe vomiting
    o ataxia
    o diplopia
    o hemi paresis
    o unilateral facial weakness
    o tinnitus
  • around 10% died on the first presentation
  • Good prognosis is patient survive.
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9
Q

What are the investigation mortality for disection carotid/vertebral

A

1) Angiography
- conventional gold standard
- invasive
- show carodit stenosis usually 2-3 cm distal to carotid bulb
2) MRI/MRA
- Repalcing angiography as the gold standard
- can show dissection and hematoma in wall

Findings

  • irregular vessel margins
  • filling defects
  • Extravasation of contrast
  • Calibre changes
  • vascular occlusion
  • intimal flaps

3) Helical CT angiography
- similar result to MRI
- sensitivity approach 100%
- More readily availability
4) Ultrasound

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10
Q

What is Cervicogenic headache?

A
  • originate from the disorder of the neck
  • based on the presence of the following 3 distinct sets of symptoms
    o 1) unilateral headache triggered by movement of head or neck or certain head position
    o 2) unilateral headache triggered by pressure on the neck
    o 3) Unilateral headache spreading to the neck or possibly the ipsilateral shoulder or arm
    Usually after a whiplash injury
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11
Q

Describe Coital Headache

A
  • recurrent benign headache associated with sexual activity
  • men more than women
  • occurs just before, during or immediately after orgasm
  • dull and throbbing
  • last from minutes to hours
  • NB explosive headache and being severe should be investigated for SAH
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12
Q

Cough and exertional headache

A
  • severe headache following a few seconds after cough, sneezing, laughing, heavy lifting or exertion
  • can be brief but can last up to 24hrs
  • Bilateral and throbbing in nature
  • NB – headache can be due to a structural lesions especially in the posterior fossa in some people and so a CT or MRI may be required
  • NSAIDs have been effective
  • Avoiding the triggering mechanism
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13
Q

What are the principle of Giant Cell Arteritis

A
  • Systemic inflammatory process of the small and medium – sized arteries.
  • Mean age of 71
  • Rare before age of 50
  • Female are more commonly affected than males
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14
Q

What are the clinical presentation of Giant Cell Arteritis

A
  • 70% develop headache often worse at night or exposure to cold
  • Sharp, throbbing, boring or aching - localized to the temporal region but can occur anywhere on the head.
  • Can be continuous or intermittent.
  • There may be tenderness on the scalp in the area and aggravated by wearing head or putting pressure on it.
  • Jaw claudication may occur due to involvement of the Masseter and temporalis
  • Weight loss + fever and anorexia.
  • 40% complain of pain in there large proximal joints especially in the morning ( polymyalgia rheumatica)
    Serious complication is loss of vision in 86% of untreated cases
  • Amaurosis fugax often occur prior to the visual loss
    Other complications – TIA, stroke, peripheral neuropathy
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15
Q

What are the diagnostic evaluation of Giant Cell Arteritis

A
  • History
  • Exam – visual examination
  • Investigation – ESR, CRP elevated LFT
  • Elevated platelet count (> 400,000)
  • Temporal artery biopsy
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16
Q

What are the treatment of Giant Cell Arteritis

A

Medical emergency

  • Steroid – 60 to 120mg/day – response occurs over days
  • Require long term management with ESR as a cage for response
17
Q

what is the priciple of high altitude headache?

A
  • cardinal manifestation of acute mountain sickness especially above 5000 feet above sea level.
  • Throbbing in temporal or occipital areas
  • Probably caused by a mild raised in ICP
  • Worse at night and early morning
  • Associated fatigue, nausea, vomiting, dizziness, insomnia
18
Q

What is the treatment for high altitude headache?

A
  • Supplementary Oxygen

- Decent to lower altitute

19
Q

What is the principle for hypertensive headache?

A
  • Sudden change of blood pressure is more important than the isolated BP itself.
  • Diastolic BP <130mmhg – BP is rarely the cause of the headache.
  • Severe hypertension is associated with headache – hypertensive encephalopathy – BP 250/150mmhg.
  • Other condition causing the severe headache like Pheochromocytoma, Eclampsia, drugs
  • diffuse, worse when awakes in the morning and settled as the day progress
  • Treatment is to reduce the BP slowly
  • Subside with 24hr or a few days if there is any edema
20
Q

What is the principle of idiopathic intracranial hypertension?

A
  • pseudo tumor cerebri or benign intracranial hypertension
  • young obese women in childbearing age
  • several predisposing factors include -:
    o anabolic steroid
    o OCP
    o Tetracycline
    o Vitamin A
21
Q

What is the pathophysiology and clinical features of Idiopathic intracranial hypertension

A
  • controversial
  • increase brain water content
  • decrease CSF outflow
  • Generalized headache / gradual onset and moderate intensity
  • Worsen by eye movement or awaken patients from sleep
  • Valsalva impedes cerebral venous return
  • Visual complaints are common – due to ischemia of visual pathway. Gradually become frequent and prolong visual loss and 10% develop permanent visual impairment
  • There may be nausea, vomiting and dizziness associated
  • Exam – papilloedema, visual field defect
    Enlarged blind spot, loss of peripheral vision
    Occasional 6th nerve palsy is noted
22
Q

How do you diagnose idiopathic intracranial hypertension

A
  • raised ICP > 200mm H2O during LP
  • sign and symptoms of raise ICP without localizing sound
  • no mass lesion or ventricular enlargement on neuro imaging
  • Normal to low CSF protein and normal cell count
  • No clinical or neuroimaging suspicion of venous sinus thrombosis
23
Q

What are the treatments of Idiopathic intracranial hypertension

A
  • discontinued meds responsible
  • lower ICP and managing the headache
  • drugs
  • Acetazolamide – decrease CSF production
  • Frusemide
  • Steroids
  • If medical therapy fail and risk loosing vision surgical management may be an option.
  • Ventricular shunt or optic nerve sheath fenestration may be indicated
24
Q

What are the Principles of medication induced headache?

A

Feature

  • women more affected
  • 30 to 40 years old
  • Accompanied by nausea, vomiting, asthenia, anxiety, and depression
  • Medication overuse headache is pre – emptive use of drug in anticipation of rather than for headache.

eg

  • NSAID
  • ASA
  • Acetaminophen
  • Barbiturate etc
  • Withdrawal of the overuse drug
  • Education and follow up program involving pharmacologic, dietary and behavioral component.
25
Q

What is the principle of disease and pathophysiology of Postdural puncture headache?

A
  • Most common complication of LP (40%)
  • highest in the 18 to 30 years of age
  • onset can be immediate or a few days after LP
  • Etiology – not clearly understood but the most likely explanation is excess CSF leak compared to rate of production. This cause the brain to descend in the cranial vault and causes traction on the pain fibers.
  • Certain factors have been implicated
  • Size of the needle
  • Orientation of the needle bevel during the procedure
  • Amount of fluid withdrawn
  • Blunt vs. sharp needle
26
Q

What are the clinical features of postdural puncture headache?

A
  • Bilateral , throbbing and exacerbated by the upright position
  • Associate symptoms include neck stiffness, nausea, vomiting, auditory disturbance including tinnitus and hearing loss (hypoacusis) and ocular symptoms like blurred vision and diplopia.
27
Q

What are the treatment of Post dural puncture headache?

A
  • resolve spontaneously within a few days, with rest + hydration and mild analgesics
  • Persistent headache use methylxanthine agents
    o Oral caffeine 300mg q 4 to 6 hrs
    o Caffeine sodium benzoate 500mg in 1 liter of fluid
  • Theophyline 300mg oral q 8hrs
  • Severe headaches lasting > 24hrs – epidural blood patch may be required. Successful in majority of the patients.
28
Q

What is SAH

A
  • is the extravasated blood within the subarachnoid space.
  • Spontaneous SAH results from the rupture of a cerebral aneurysm is ~85% of cases.
  • Aneurysmal SAH is most common in 40-60 yrs.
29
Q

What are the aetiology of SAH

A

85% aneurysms anterior circle
30% jx ant cerebral and com.
25% jx ic and post com.
25% bifurcation of ic

30
Q

What are the risk factors for SAH?

A
  • Smoking (2-10xs),
  • 1st degree relatives (present in 5-20%, 4xs),
  • HT,
  • heritable connective tissue disorders (eg polycystic kidney and neurofibromatosis, alpha-1 antitrypsin, Marfans)
31
Q

What are the prognosis of SAH?

A

50% die or are permantly disabled by initial event.
12% die before hospital
30% die without treatment

32
Q

What are the history of SAH

A

● 95% present with headache. Typically sudden onset and severe.
● 40-80% have a sentinel haemorrhage hours to days before and often settles spontaneously.
● Upper neck pain is common.
● 1/3 will develop SAH on strenuous exercise.
● Nausea and vomiting in 75%
● Brief (cerebral perfusion pressure decreases at time of bleed as ICP approaches MAP) or permanent LOC occurs in majority.
● Seizures in 15%

33
Q

What are the clinical findings of SAH?

A

● Signs of meningism in 75% (may be late).
● Focal neurology in 25% (assoc intracranial haemmorhage, vasospasm, nerve compression (eg 3rd CN by post comm and ic aneurysm), or raised ICP (6th nerve – cavernous sinus)
● Grading by two scales: Hunt and Hess, and World Federation of Neurosurgeons.

34
Q

What are the Investigations for SAH?

A

● Non-contrast brain CT. In 1st 24 hours will be +ve 90-95% of the time. Sensitivity decreases with time: 80% at 3 days and 50% at 1 week. CT will also help with possible location, extent of haemorrhage, demonstrates hydrocephalus.
● LP needed if there is clinical suspicion and the CT is -ve, inadequate, or equivocal.
● >100 000 RCC is indicative of SAH.
● Xanthochromia present after 4 hrs, in all cases > 12 hours, persists 2 weeks. Not present in traumatic tap.
● Cerebral Angiography – Will show multiple aneurysms in 25%. Defines anatomic details and presence of vasospasm. Will show AV malformation
● ECG – Non-specific changes are common eg. May mimic ischaemia, esp inferiorly, widened QRS, prolonged QT, peaked or deeply inverted T-waves

35
Q

What are the prognostic indicator for SAH?

A

GradeI asymptomatic or minor headache with mild nuchal rigidity
Grade III Drowsiness, confusion, mild focal deficit
Grade V Deep coma, decerebrate, moribund

36
Q

What are the management for SAH?

A

+ ABC’s
+ Supportive care
+ Antiemetics
+ Reduction of raised ICP (eg. head up max,
- PaCO2 35-45mmHg),
- MAP 80-100
+ Nimodipine gt 60mg q4h (or up to 2mg/hr IV if needed)
+ Maintenance fluids 5% dex to main normal/high osmolality

As a rule: minimal sedation for ongoing assessment eg. Propofol infusion 50-150mg/hr

+ NBB - If M4 or better: angio at 1st convenient time
+ NBB - If M3 or less: SEP’s and repeat CT. Surgery usually deferred.
- EVD: inserted if CT scan looks ‘tight’ or fail to improve neurologically.
- 1G Flucloxacillin given before insertion.
++ Surgical clipping: I or II within 48 hours
- Interventional radiology: detachable coil embolisation

37
Q

What are the delayed effects

A 
a) Re - Bleed
●	10-30% will rebleed
●	usually in first 3-5 days
●	50% mortality
Vasospasm and delayed neurological deficit
●	incidence 30%
●	Usually between days 4-14
●	30% die and 30% have permanent deficit
●	occurs in response to the breakdown products of blood in the SA space
38
Q

What are the principle of Trigeminal Neuralgia

A
  • unilateral pain affecting face
  • Characterized by electric shock like pain
  • Follow the distribution of branch/s of trigeminal nerve
  • Pain is evoked by trivial stimuli – washing, shaving, smoking etc
  • Attacks are brief from few seconds to few minutes
  • Diagnosis is straight forward but for the first time sufferer it can also represent an underlying mass lesion – CT or MRI is indicated.
39
Q

What are the teratments dor Trigeminal neuralgia?

A
  • unilateral pain affecting face
  • Characterized by electric shock like pain
  • Follow the distribution of branch/s of trigeminal nerve
  • Pain is evoked by trivial stimuli – washing, shaving, smoking etc
  • Attacks are brief from few seconds to few minutes
  • Diagnosis is straight forward but for the first time sufferer it can also represent an underlying mass lesion – CT or MRI is indicated.

Neurology (17 decks)

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