20. Headache Flashcards

1
Q

DDX headache

A

Vascular:
Migraine
Haemorrhage (EDH,SDH, SAH, ICH)

Infective/immune:
Meningitis
Encephalitis
Abscess
Herpes zoster
Sinusitis

Trauma
SAH
SAH → hydrocephalus
EDH
SDH

Autoimmune
Temporal arteritis

Iatrogenic
Medication overuse
Post lumbar puncture

Idiopathic
Idiopathic intracranial hypertension
Tension headache
Cluster headache
Trigeminal neuralgia
Hypertension/malignant HTN

Neoplastic
Glioma
Meningioma
Pheochromocytoma
Space occupying lesion → hydrocephalus

Congenital
Hydrocephalus

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2
Q

History taking headache

A

PC: SOCRATES
hoPC: recent trauma? Recent illness? lacrimation?, headache behaviour? lacrimation?
Red flags: fever, weight loss, worse in morning, worse on coughing, worse on straining, vomiting, weakness, sensation etc. photophobia, associated non-blanching rash, vision changes? Aura? Nausea and vomiting? confusion?
MHx: history of cancer? Immunocompromised? HIV?
DHx: pain killers? Immunosuppressive drugs?
FHx:
SHx: household contacts with same issue? (carbon monoxide poisoning)
ICE:

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3
Q

Examination headache

A

Vital signs — assess blood pressure, pulse, respiration rate, temperature, and oxygen saturation levels.

General appearance and mental state — assess for signs of a serious underlying cause, including non-blanching skin rash, reduced level of consciousness, or confusion.

Extracranial structures — assess the carotid arteries, temporal arteries, sinuses, and temporomandibular joints.

The neck — assess for meningeal irritation, tenderness of cervical paraspinal muscles, range of movement, and crepitation, neck pain - acute torticollis, Neck pain - cervical radiculopathy

Fundoscopy — assess for papilloedema, pupillary asymmetry and reactivity.
Neurological examination — assess cranial and peripheral nerves including gait.

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4
Q

Recurrent, severe headache which is unilateral and throbbing in nature. Associated with nausea and photosensitivity. Last 4-72 hours
Behaviour: withdrawal, not moving, dark room, no noise

A

migraine

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5
Q

Typical history migraine

A

PC: Recurrent, severe headache which is unilateral and throbbing in nature. Associated with nausea and photosensitivity. Last 4-72 hours
Behaviour: withdrawal, not moving, dark room, no noise

DHx: COCP
SHx: alcohol, caffiene, chocolate, cheese, travel

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6
Q

Migraine triggers

A

Mneumonic CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese/Caffeine
Oral contraceptive pill
Lie-ins
Alcohol
Travel
Exercise

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7
Q

Migraine diagnostic criteria

A

A. At least 5 attacks fulfilling criteria B-D

B. Between 4-72 hours* (untreated or unsuccessfully treated)

C. Characteristics, 2 of:
1. unilateral location*
2. pulsating quality (i.e., varying with the heartbeat)
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)

D. During headache at least one of the following:
1. nausea and/or vomiting*
2. photophobia and phonophobia

E. Everything else excluded

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8
Q

Acute treatment of migraine

A

In practice:
1. combination therapy triptan + NSAID
2. Add in an anti-emetic - metoclopramide 10mg or prochlorperazine 10mg
+ use non-oral preparations of the above if vomiting is an issue

depending on severity use:
Simple analgesia
- Ibuprofen (400 mg) — if ineffective, consider increasing to 600 mg or
- Aspirin (900 mg) or
- Paracetamol (1000 mg).

Triptan
- sumatriptan (50–100 mg)

Anti-emetic
- metoclopramide 10mg or prochlorperazine 10mg

Warn pts about medication overuse headache..

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9
Q

criteria for getting migraine prophylaxis

A

‘Migraine attacks are having a significant impact on quality of life and daily function, for example they occur frequently (more than once a week on average) or are prolonged and severe despite optimal acute treatment’

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10
Q

Migraine prophylaxis

A

Women
1. Propranolol or amitriptyline

Men
1. Topiramate or amitriptyline

  1. Accupuncture up to 10 sessions of acupuncture over 5-8 weeks’
  • riboflavin can be effective in reducing migraine frequency
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11
Q

How to treat pre-menstrual migraine

A

Frovatriptan (2.5mg twice a day) or zolmitriptan (2.5mg twice or three times a day) as mini-prophylaxis

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12
Q

What type of side effects can occur in children and young adults taking antiemetic metoclopramide?

A

EPSE (extrapyramidal side effects)

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13
Q

Typical history SAH

A

PC: Sudden onset occipital headache (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death

HoPC: head injury (traumatic SAH)
MHx: autosomal dominant polycystic kidney disease, ehlers-danlos, coarctation of aorta (all associated with intercranial aneurysm)

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14
Q

Sudden onset occipital headache (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death

A

SAH

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15
Q

Most common cause SAH

A

head injury

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16
Q

conditions which increase likelihood of cerebral aneurysm

A

adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta

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17
Q

Plan ?SAH

A

Plan
Invetsigations
1. CT head (Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system) convex shape

  1. Lumbar puncture used to confirm SAH if Ct negative, perfomed at least 12 hours after onset, xanthochromia seen

Management
1. referral to neurosurgery
risk of rebleeding so treat promptly
1. Coil by interventional radiologist
2. Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature)
3. Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt

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18
Q

Complications of SAH

A
  • re-bleeding
  • vasospasnm
  • hyponautraemia caused by SIADH
  • seizures
  • hydrocephalus
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19
Q

Typical history meningitis inc neonates

A

Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash

Neonates:
Hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.

Therefore lumbar puncture in all children if:
Under 1 month old and presenting with fever
1-3 months with fever and unwell
Under 1 years with unexplained fever and other features of serious illness

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20
Q

Examination findings meningitis

A

Fever
Non-blanching rash
Photophobia

Kernig’s test (Kernig’s test involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.)
Brudzinski test (Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.)

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21
Q

What is Meningococcal meningitis vs Meningococcal septicaemia

A

Meningococcal meningitis - meningococcus bacteria (neisseria meningitidis) is infecting the meninges and CSF

Meningococcal septicaemia - meningococcal bacterial infection in the bloodstream → non blanching rash due to DIC and subcutaneous haemorrhage

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22
Q

plan ?meningitis

A

Airway
Breathing
Circulation
Disability: GCS, ; focal neurological signs; seizures; papilloedema;

Initial:
if in primary care and ?meningococcal - an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important:
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg

Once in hospital, decisions to treat empirically quickly vs LP depends on patient and senior clinician

Investigations:
Bloods:
full blood count
CRP
coagulation screen
blood culture
whole-blood PCR, this will be relied upon if lumbar puncture contraindicated
blood glucose
blood gas

Lumbar puncture
unless contraindicated eg if there is evidence of raised ICP as it can cause herniation of cerebrum. Signs of raised ICP: cushing’s reflex (raised BP, low HR), focal neurological signs, papilloedema, significant bulging of the fontanelle, disseminated intravascular coagulation (meningococcal septicaemia eg the rash), signs of cerebral herniation.

Blood glucose at same time as CSF so can be compared

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23
Q

Normal lumbar puncture result

A

clear appearance

glucose 70% of plasma

protein 0.3 g/l

WCC 2 per mm^3 (neuts)

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24
Q

Bacterial meningitis LP result

A

Cloudy

Glucose low (< 1/2 plasma) bacteria using up the glucose

Protein high (> 1 g/l) bacteria releasing proteins

WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria

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25
Q

Viral meningitis LP result

A

Clear/cloudy

Glucose 60-80% of plasma glucose* viruses don’t really use glucose

Protein normal/raised viruses may release a small amount of protein

WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses

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26
Q

Tuberculous LP result

A

Slight cloudy, fibrin web

glucose Low (< 1/2 plasma)

Protein high >1g/l

WCC 30-300 lymphocytes/mm3

The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)

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27
Q

Bacterial meningitis 0-3 months

A

BELS

  1. Group B Streptococcus (most common cause in neonates)
  2. E. coli
  3. Listeria monocytogenes
  4. Strep pneumoniae
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28
Q

Bacterial meningitis 3 months-6 years

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
  3. Haemophilus influenzae
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29
Q

Bacterial meningitis 6-60 years

A
  1. Neisseria meningitidis
  2. Streptococcus pneumoniae
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30
Q

Bacterial meningitis >60 years

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis
  3. Listeria monocytogenes
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31
Q

Meningitis in immunocompromised

A

listeria monocytogenes

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32
Q

Community meningitis initial management

A

Benzylpenicillin IM or IV

< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg

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33
Q

Meningitis initial empirical therapy < 3 months

A

IV cefotaxime + amoxicillin (or ampicillin)

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34
Q

Meningitis initial empirical therapy 3 months-50 years

A

IV cefotaxime

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35
Q

Meningitis initial empirical therapy > 50 years

A

IV cefotaxime + amoxicillin (or ampicillin)

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36
Q

Meningitis management - listeria

A

IV amoxicillin (or ampicillin)
+ gentamicin

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37
Q

When should dexamethasone be given for meningitis?when should it be withheld?

A

Give if lumbar puncture reveals:
- frankly purulent CSF
-CSF white blood cell count greater than 1000/microlitre
- raised CSF white blood cell count with protein concentration greater than 1 g/litre
- bacteria on Gram stain

Withhold if:
- septic shock
- meningococcal
- septicaemia
immunocompromised

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38
Q

Management meningococcal meningitis

A

IV benzylpenicillin or cefotaxime

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39
Q

Post exposure prophylaxis bacterial meningitis

A

Ciprofloxacin single dose

This risk is highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness

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40
Q

Typical history encephalitis

A

PC:
Fever
Headache
Confusion

  • psychiatric symptoms
  • vomiting
  • seizures
  • focal features
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41
Q

Brain scan where does encephalitis classically affect

A

temporal lobe

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42
Q

Most common pathogen encephalitis in children and adults

A

herpes simplex HSV-1 from cold sores

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43
Q

Most common pathogen encephalitis in neonates

A

herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.

think “been passed on 2”

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44
Q

Plan ?encephalitis

A

Initial:
Immediate IV aciclovir (covers HSV and varicella zoster)

Invetsigations:
- CSF : lymphocytosis, raised protein
- PCR for HSV
- CT medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients.
- MRI is better
- EEG pattern: lateralised periodic discharges at 2 Hz

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45
Q

Management CMV encephalitis

A

Ganciclovir

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46
Q

Typical history brain abscess

A

PC:
- dull persistant headache
- fever
- focal neurology
- features of raised ICP

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47
Q

Plan ?brain abscess

A

Invetsigation:
- CT may be useful
- diffusion weighted mri is best
- invetsigate for sepsis and ddx etc

Management:
1. surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.

  1. IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
  2. intracranial pressure management: e.g. dexamethasone
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48
Q

Typical history herpes zoster opthalmicus

A

vesicular rash around the eye, which may or may not involve the actual eye itself, burning sensation around eye

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49
Q

what is herpes zoster opthalmicus

A

the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve.

It accounts for around 10% of case of shingles.

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50
Q

Plan ?herpes zoster opthalmicus

A

Management
1. oral antiviral treatment for 7-10 days

+. topical corticosteroids may be used to treat any secondary inflammation of the eye

+ocular involvement requires urgent ophthalmology review

51
Q

Complications herpes zoster opthalmicus

A

ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia

52
Q

typical history sinusitis

A

PC: Facial ‘fullness’ and tenderness
Purulent nasal discharge, pyrexia or post-nasal drip leading to cough, nasal obstruction

53
Q

plan ?sinusitis

A

Management
1. analgesia

> 10 days
1. Intranasal corticosteroids
+ abx if severe
1. pen V
2. Co-amox if systemically unwell

54
Q

Typical history temporal arteritis

A

Typically patient > 60 years old
PC: Usually rapid onset (e.g. < 1 month) of unilateral headache
- worse when talking for a while, worse when chewing, worse when moving jaw, tender to touch, scalp tenderness, worse when brushing hair, shaving etc

Red flags: visual disturbance, Amaurosis fugax, Blurring, Double vision

MHx: Polymyalgia rheumatica:
50% have features of PMR : aching, morning stiffness in proximal limb muscles

o/e: Tender, palpable temporal artery

55
Q

Pathophysiology temporal arteritis

A

Type of large cell vasculitis
Autoimmune

56
Q

Plan ?temporal arteritis

A

medical emergency due to risk of
- stroke
- blindness (a strple affecting the retinal vessels, optic nerve) - 90% AION (Anterior Ischemic Optic Neuropathy)

phone rheum on-call

Should have confirmatory test: USS halo sign or temporal artery biopsy
also get ESR

Initial
1. High dose oral glucocorticoids eg oral methylprednisolone

With visual loss:
1. IV methylprednisolone
+ Urgent ophthalmology review
+ Bone protection for steroids

refractory/relapsing : tocilizumab

57
Q

typical presentation of post lumbar puncture headache

A

usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position

58
Q

Plan ?post LP headache

A
  1. Caffeine and fluids
    supportive initially (analgesia, rest)
  2. if pain continues for more than 72 hours then specific treatment is indicated, to prevent subdural haematoma
    treatment options include: blood patch, epidural saline and intravenous caffeine
59
Q

Typical history idiopathic intracranial HTN

A

Young female

PC:
Headache
Blurred vision
Vision : Transient visual obscuration, Enlargement of the blind spots and circumferential restriction in visual fields

o/e:
Papilloedema
Enlarged blind spot
Sixth nerve palsy may be present

MHx: obesity, pregnancy
DHx: OCP, lithium, vitamin A, levothyroxine, isoretinoin, steroids, tetracyclines, doxycycline

60
Q

Plan ?IIH

A

Examination
1. fundoscopy: papilloedema
2. CN exam

Invetsigation:
Exclude other causes of raised icp eg scans
Lumbar puncture? - raised opening pressure normal reference range 5-25 cmH2O

Management:
1. weight loss
2. diuretics e.g. acetazolamide
3. topiramate is also used, and has the added benefit of causing weight loss in most patients

repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management

surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.

A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

61
Q

Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living

A

tension headache

62
Q

Typical history cluster headache

A

PC: Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
HoPC: Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers
nasal stuffiness
miosis and ptosis in a minority
Behaviour: agitation, strange ways to cope eg shouting, banging head against wall

SHx: smoking and alcohol and poor sleep

63
Q

Plan ?cluster headache
acute and LT

A

Acute:
1. subcutaneous triptan - intranasal in gp (75% response within 15 mins)
(triptans are contraindicated in CAD as it may cause vasospasm)
2. 100% high flow oxygen (80% response within 15 mins)

Prophylaxis:
1. Verapamil
(2. tapering dose of prednisolone)

64
Q

Most common cancers to metastasise to the brain?

A

brain = 2 hemishpheres so to remember spread..

Things you have 2 of:
Lung (most common)
Breast
Renal cell carcinoma/Kidney

then 2 left:
Melanoma
Bowel

65
Q

What are gliomas? grades?

A

Tumours of the glial cells in the brain or spinal cord
Glial cells provide support and nutrients for neurones

Grade 1
Pilocytic astrocytoma (usually paeds)
Grade 2
Low grade glioma
Grade 3
Malignant glioma
Grade 4
Glioblastoma multiforme (most common and most aggressive)

66
Q

what is the most common primary brain tumour in children?

A

pilocytic astrocytoma

67
Q

typical history pilocytic astrocytoma

A

PC: headache w raised icp features, n&v, abnormalities of gait and coordination, papilloedema

68
Q

what is the most common primary brain tumour in adults

A

glioblastoma multiforme

69
Q

Typical history glioblastoma multiforme

A

PC: Headache - typically worse on waking, Nausea and vomiting.Seizures - especially low-grade astrocytomas.Visual disturbance.
Speech and language problems.Changes in cognitive and/or functional ability.
MHx: NFT1

70
Q

plan ?glioblastoma multiforme + investigation findings

A

Plan

Investigation
Urgent (2ww) direct access MRI (or CT if contraindicated)
Imaging: solid tumours with central necrosis and a rim that enhances with contrast
Histology: Pleomorphic tumour cells border necrotic areas

Management
1. Surgery
+ Postoperative chemotherapy and/or radiotherapy
+ Dexamethasone is used to treat oedema.

71
Q

solid tumours with central necrosis and a rim that enhances with contrast

A

glioblastoma

ddx brain abscess

72
Q

A CT head with contrast reveals a rim-enhancing lesion with a central cavity and surrounding oedema

A

brain abscess

ddx glioblastoma

73
Q

what are meningiomas?

A

Meningiomas are tumours growing from the cells of the meninges in the brain and spinal cord.

They are usually benign, however they can take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms

74
Q

where do meningiomas arise from? located?

A

They arise from the arachnoid cap cells of the dura of the meninges and are typically located next to the dura

They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base

75
Q

Typical history meningioma

A

PC: raised icp headaches, seizures, neuropsychological eg disinhibition, neuro features

76
Q

Plan ?meningioma

A

MRI

Management
Observation, radiotherapy, surgical resection

77
Q

what is a pheochromocytoma

A

A phaeochromocytoma (PCC) is a rare tumour that secretes catecholamines. It is derived from chromaffin cells, usually in the adrenal medulla
The excessive production of catecholamines may cause life-threatening hypertension or cardiac arrhythmias. Undiagnosed phaeochromocytomas, whether or not subclinical and even if biologically benign, may cause extremely deleterious consequences or even death, following abrupt release of catecholamines.

78
Q

typical history pheochromocytoma

A

PC: Headache, Profuse sweating, Palpitations, Tremor
o/e: HTN, postural hypotension, tremor

79
Q

plan ?pheochromocytoma

A

Plan
Investigations
24-hour urine collection for metanephrines
plasma catecholamines

Management:

If HTN crisis
Phentolamine IV (alpha blocker)

Non-HTN crisis
Alpha blocker eg phenoxybenzamine: 10 mg orally twice daily initially, increase by 10 mg/day increments every other day according to response, maximum 240 mg/day (alpha blocker)
+ beta blocker

Then surgery

80
Q

what is hydrocephalus

A

Hydrocephalus is defined as a condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain.

81
Q

types of hydrocephalus

A

obstructive - structural pathology blocking the flow of cerebrospinal fluid

non-obstructive - imbalance of CSF production absorption. It is either caused by an increased production of CSF (e.g. choroid plexus tumour (very rare)) or more commonly a failure of reabsorption at the arachnoid granulations (e.g. meningitis or post-haemorrhagic)

82
Q

causes of obstructive hydrocephalus

A

tumours

acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage)

developmental abnormalities (e.g. aqueduct stenosis).

83
Q

causes of non-obstructive hydrocephalus

A

choroid plexus tumour

meningitis

post-haemorrhagic

Normal pressure hydrocephalus

84
Q

presentation hydrocephalus

A

PC:
Headache (typically worse in the morning, when lying down and during valsalva)
Nausea and vomiting
Papilloedema
Coma (in severe cases)

o/e:
Infants:
Increased head circumference
Sunsetting eyes (defective upward gaze)
Bradycardia
Seizures
Coma

85
Q

Plan ?hydrocephalus

A

Investigation
1. CT as quick
2. MRI as more detail eg if lesion
3. Lumbar puncture for non-obstructive is both diagnostic and therapeutic

Management
1. treat underlying cause
1. external ventrictlar drain (temporary)
2. ventriculoperitoneal shunt (long-term)

86
Q

Typical history medication overuse headache

A

PC: headache for 15 days per month
DHx: simple analgesics, triptans, opiod analgesia

87
Q

management medication overuse headache

A

simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)

opioid analgesics should be gradually withdrawn

88
Q

what is papilloedema?

A

Papilloedema is a swelling of the optic disc secondary to raised intracranial pressure. Papill- refers to a small rounded raised area (the optic disc) and -oedema refers to the swelling.

It can be tricky to learn to recognise papilloedema. When looking for elevation of the optic disc, look at the way the retinal vessels flow across the disc. Vessels are able to flow straight across a flat surface, whereas they will curve over a raised disc.

89
Q

what is cushings reflex

A

irregular breathing, bradycardia, widening pulse pressure (blood pressure)

90
Q

normal icp opening pressure

A

7-15 mmHg in adults in the supine position

91
Q

causes of raised icp

A

Space occupying lesion
Bleed
IIH (idiopathic intracranial hypertension)
Traumatic head injuries
Hydrocephalus
Infection eg meningitis

92
Q

plan ?raised icp

A

investigation
1. CT head
2. blood culture, whole blood pcr etc for infection

Management
1. treat underlying cause

head elevation to 30º

IV mannitol may be used as an osmotic diuretic

controlled hyperventilation

removal of CSF, different techniques include:
drain from intraventricular monitor (see above)
repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
ventriculoperitoneal shunt (for hydrocephalus)

93
Q

how does controlled hyperventilation reduce icp

A

aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain

94
Q

Severe unilateral pain, often triggered by touching the skin, brief electric shock like pains, abrupt in onset and termination

A

trigeminal neuralgia

95
Q

triggers trigeminal neuralgia

A

Light touch, washing, shaving, mocking, talking, brushing teeth. Particularly of nasolabial fold.

96
Q

Causes trigeminal neuralgia

A

Classical trigeminal neuralgia is caused by pressure on the trigeminal nerve close to where it enters the brain stem. Most cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems could be the cause.

97
Q

red flags for non-idiopathic cause of trigeminal neuralgia

A

Red flags:
Sensory changes
Deafness or other ear problems
History of skin or oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years

98
Q

management trigeminal neuralgia

A

Carbamazepine

99
Q

ct scan findings SAH

A

Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

“star sign”

100
Q

may have lucid interval (hours) between trauma and presentation, features of raised ICP

A

extradural haemorrhage

101
Q

cause EDH

A

typically caused by blunt-force, low-impact traumatic head injury. Patients may regain consciousness initially following the injury but progressively slip into a coma as the haematoma continues to expand.

Majority occur in temporal region where skull fractures and causes a rupture of the middle meningeal artery

102
Q

Presentation extradural hematoma

A

trauma LOC –> lucid interval –> herniation –> LOC and surgical third nerve palsy

103
Q

management of extradural hematoma

A

stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.

104
Q

blood vessel implicated by extradural hematoma

A

middle meningeal artery

eminem getting hit by a lemon

105
Q

ct scan subdural hematoma

A

concave crescent-shaped

hyperdense (bright)= acute
hypodense (dark) = chronic

106
Q

blood vessel implicated in subdural hematoma

A

bridging veins

old man drinking alcohol in a cave with a bridge outside and a crescent moon in the sky

107
Q

management subdural hematoma

A

Small or incidental acute subdurals can be observed conservatively.

If big or signs then surgical options include monitoring of intracranial pressure and decompressive craniectomy with burr holes.

108
Q

presentation of acute SDH

A

typically caused by high-impact injuries (such as a road traffic accident or severe fall) and is often accompanied with diffuse injuries (such as diffuse axonal injury). Patients are either comatose from the outset and do not have the classical lucid interval that is seen in patients with extradural haematomas.

109
Q

presentation of chronic SDH

A

Most likely present 4-7 weeks following the insult and can present with a wide variety of different neurological symptoms. They are caused by an initial injury, which causes bleeding and inflammation, which becomes superseded by fibrosis and angiogenesis. This angiogenesis produces fragile leaky blood vessels, which causes blood to slowly continue to accumulate even after the injury.

110
Q

Presentation of hemorrhagic stroke

A

similar to ischaemic stroke OR reduced consciousness

May display:
- N&V
- headache
- reduced GCS

111
Q

CT haemorrhagic stroke

A

hyperdensity (bright lesion) within the substance of the brain.

112
Q

causes of ICHaemorrgage

A

Hypertension (most common)

Metastasis
Vascular malformations (AVLs)
Sinus venous thrombosis

113
Q

management of ICHaemorrahage

A
  1. Neurosurgical consultation should be considered for advice on further management. The vast majority of patients however are not suitable for surgical intervention.
  2. Management is therefore supportive as per haemorrhagic stroke. Anticoagulants (e.g. warfarin) and antithrombotic medications (e.g. clopidogrel) should be stopped to minimise further bleeding.
  3. If a patient is anticoagulated this should be reversed as quickly as possible.
  4. Trials have shown improved outcomes in patients who have their blood pressure lowered acutely and this is now part of many protocols for hemorrhagic strokes.
114
Q

is mannitol used in ICH

A

although mannitol decreases edema in ICH at first,, it finally widens ICH, thus, its use is not recommended

115
Q

what does aura classically present with?

A

gradually enlarging, frequently bilateral, zigzag fortification spectra usually followed by a headache.

116
Q

Signs of raised ICP

A

cushing’s reflex (raised BP, low HR) irregular breathing, bradycardia, widening pulse pressure (blood pressure)

focal neurological signs
papilloedema
significant bulging of the fontanelle

117
Q

most common causes viral meningitis

A

echovirus, coxsackievirus

118
Q

management viral meningitis

A

supportive,

if HSV suspected - aciclovir

119
Q

Complications of meningitis

A

Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits such as limb weakness or spasticity

120
Q

contraindications to LP

A

Brain - raised ICP, convulsions, focal neurology
- reduced or fluctuating level of consciousness (Glasgow Coma Scale score less than 9 or a drop of 3 or more)
- age-relative bradycardia and hypertension
- focal neurological signs
- abnormal posture or posturing
- unequal, dilated or poorly responsive pupils
- papilloedema
- abnormal ‘doll’s eye’ movements
- tense, bulging fontanelle

Cardio - shock

Respiratory - respiratory insufficiency (lumbar puncture is considered to have a high risk of precipitating respiratory failure in the presence of respiratory insufficiency).

Blood - Coagulation abnormality
- coagulation results (if obtained) outside the normal range
- platelet count below 100×109/litre
- receiving anticoagulant therapy

121
Q

USS giant cell/temporal arteritis

A

halo sign

122
Q

features of carbon monoxide posioning

A

headache: 90% of cases
nausea and vomiting: 50%
vertigo: 50%
confusion: 30%
subjective weakness: 20%
severe toxicity: ‘pink’ skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death

123
Q

invetsigation CO posioning

A

venous or arterial blood gas should be taken
typical carboxyhaemoglobin levels
< 3% non-smokers
< 10% smokers
10 - 30% symptomatic: headache, vomiting
> 30% severe toxicity
an ECG is a useful supplementary investgation to look for cardiac ischaemia

124
Q

Management CO poisoning

A

100% high-flow oxygen via a non-rebreather mask

should be administered as soon as possible, with treatment continuing for a minimum of six hours
target oxygen saturations are 100%
treatment is generally continued until all symptoms have resolved, rather than monitoring CO levels