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Core clinical problems > 20. Headache > Flashcards

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
Viral meningitis LP result
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
26
Tuberculous LP result
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%)
27
Bacterial meningitis 0-3 months
BELS 1. Group B Streptococcus (most common cause in neonates) 2. E. coli 3. Listeria monocytogenes 4. Strep pneumoniae
28
Bacterial meningitis 3 months-6 years
1. Neisseria meningitidis 2. Streptococcus pneumoniae 3. Haemophilus influenzae
29
Bacterial meningitis 6-60 years
1. Neisseria meningitidis 2. Streptococcus pneumoniae
30
Bacterial meningitis >60 years
1. Streptococcus pneumoniae 2. Neisseria meningitidis 3. Listeria monocytogenes
31
Meningitis in immunocompromised
listeria monocytogenes
32
Community meningitis initial management
Benzylpenicillin IM or IV < 1 year – 300mg 1-9 years – 600mg > 10 years and adults – 1200mg
33
Meningitis initial empirical therapy < 3 months
IV cefotaxime + amoxicillin (or ampicillin)
34
Meningitis initial empirical therapy 3 months-50 years
IV cefotaxime
35
Meningitis initial empirical therapy > 50 years
IV cefotaxime + amoxicillin (or ampicillin)
36
Meningitis management - listeria
IV amoxicillin (or ampicillin) + gentamicin
37
When should dexamethasone be given for meningitis?when should it be withheld?
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
38
Management meningococcal meningitis
IV benzylpenicillin or cefotaxime
39
Post exposure prophylaxis bacterial meningitis
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
40
Typical history encephalitis
PC: Fever Headache Confusion - psychiatric symptoms - vomiting - seizures - focal features
41
Brain scan where does encephalitis classically affect
temporal lobe
42
Most common pathogen encephalitis in children and adults
herpes simplex HSV-1 from cold sores
43
Most common pathogen encephalitis in neonates
herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth. think "been passed on 2"
44
Plan ?encephalitis
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
45
Management CMV encephalitis
Ganciclovir
46
Typical history brain abscess
PC: - dull persistant headache - fever - focal neurology - features of raised ICP
47
Plan ?brain abscess
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 1. intracranial pressure management: e.g. dexamethasone
48
Typical history herpes zoster opthalmicus
vesicular rash around the eye, which may or may not involve the actual eye itself, burning sensation around eye
49
what is herpes zoster opthalmicus
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.
50
Plan ?herpes zoster opthalmicus
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
Complications herpes zoster opthalmicus
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis ptosis post-herpetic neuralgia
52
typical history sinusitis
PC: Facial 'fullness' and tenderness Purulent nasal discharge, pyrexia or post-nasal drip leading to cough, nasal obstruction
53
plan ?sinusitis
Management 1. analgesia > 10 days 1. Intranasal corticosteroids + abx if severe 1. pen V 2. Co-amox if systemically unwell
54
Typical history temporal arteritis
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
Pathophysiology temporal arteritis
Type of large cell vasculitis Autoimmune
56
Plan ?temporal arteritis
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
typical presentation of post lumbar puncture headache
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
Plan ?post LP headache
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
Typical history idiopathic intracranial HTN
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
Plan ?IIH
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
Recurrent, non-disabling, bilateral headache, often described as a 'tight-band' Not aggravated by routine activities of daily living
tension headache
62
Typical history cluster headache
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
Plan ?cluster headache acute and LT
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
Most common cancers to metastasise to the brain?
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
What are gliomas? grades?
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
what is the most common primary brain tumour in children?
pilocytic astrocytoma
67
typical history pilocytic astrocytoma
PC: headache w raised icp features, n&v, abnormalities of gait and coordination, papilloedema
68
what is the most common primary brain tumour in adults
glioblastoma multiforme
69
Typical history glioblastoma multiforme
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
plan ?glioblastoma multiforme + investigation findings
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
solid tumours with central necrosis and a rim that enhances with contrast
glioblastoma ddx brain abscess
72
A CT head with contrast reveals a rim-enhancing lesion with a central cavity and surrounding oedema
brain abscess ddx glioblastoma
73
what are meningiomas?
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
where do meningiomas arise from? located?
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
Typical history meningioma
PC: raised icp headaches, seizures, neuropsychological eg disinhibition, neuro features
76
Plan ?meningioma
MRI Management Observation, radiotherapy, surgical resection
77
what is a pheochromocytoma
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
typical history pheochromocytoma
PC: Headache, Profuse sweating, Palpitations, Tremor o/e: HTN, postural hypotension, tremor
79
plan ?pheochromocytoma
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
what is hydrocephalus
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
types of hydrocephalus
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
causes of obstructive hydrocephalus
tumours acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage) developmental abnormalities (e.g. aqueduct stenosis).
83
causes of non-obstructive hydrocephalus
choroid plexus tumour meningitis post-haemorrhagic Normal pressure hydrocephalus
84
presentation hydrocephalus
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
Plan ?hydrocephalus
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
Typical history medication overuse headache
PC: headache for 15 days per month DHx: simple analgesics, triptans, opiod analgesia
87
management medication overuse headache
simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches) opioid analgesics should be gradually withdrawn
88
what is papilloedema?
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
what is cushings reflex
irregular breathing, bradycardia, widening pulse pressure (blood pressure)
90
normal icp opening pressure
7-15 mmHg in adults in the supine position
91
causes of raised icp
Space occupying lesion Bleed IIH (idiopathic intracranial hypertension) Traumatic head injuries Hydrocephalus Infection eg meningitis
92
plan ?raised icp
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
how does controlled hyperventilation reduce icp
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
Severe unilateral pain, often triggered by touching the skin, brief electric shock like pains, abrupt in onset and termination
trigeminal neuralgia
95
triggers trigeminal neuralgia
Light touch, washing, shaving, mocking, talking, brushing teeth. Particularly of nasolabial fold.
96
Causes trigeminal neuralgia
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
red flags for non-idiopathic cause of trigeminal neuralgia
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
management trigeminal neuralgia
Carbamazepine
99
ct scan findings SAH
Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system. "star sign"
100
may have lucid interval (hours) between trauma and presentation, features of raised ICP
extradural haemorrhage
101
cause EDH
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
Presentation extradural hematoma
trauma LOC --> lucid interval --> herniation --> LOC and surgical third nerve palsy
103
management of extradural hematoma
stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.
104
blood vessel implicated by extradural hematoma
middle meningeal artery eminem getting hit by a lemon
105
ct scan subdural hematoma
concave crescent-shaped hyperdense (bright)= acute hypodense (dark) = chronic
106
blood vessel implicated in subdural hematoma
bridging veins old man drinking alcohol in a cave with a bridge outside and a crescent moon in the sky
107
management subdural hematoma
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
presentation of acute SDH
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
presentation of chronic SDH
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
Presentation of hemorrhagic stroke
similar to ischaemic stroke OR reduced consciousness May display: - N&V - headache - reduced GCS
111
CT haemorrhagic stroke
hyperdensity (bright lesion) within the substance of the brain.
112
causes of ICHaemorrgage
Hypertension (most common) Metastasis Vascular malformations (AVLs) Sinus venous thrombosis
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management of ICHaemorrahage
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.
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is mannitol used in ICH
although mannitol decreases edema in ICH at first,, it finally widens ICH, thus, its use is not recommended
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what does aura classically present with?
gradually enlarging, frequently bilateral, zigzag fortification spectra usually followed by a headache.
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Signs of raised ICP
cushing's reflex (raised BP, low HR) irregular breathing, bradycardia, widening pulse pressure (blood pressure) focal neurological signs papilloedema significant bulging of the fontanelle
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most common causes viral meningitis
echovirus, coxsackievirus
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management viral meningitis
supportive, if HSV suspected - aciclovir
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Complications of meningitis
Hearing loss Seizures and epilepsy Cognitive impairment and learning disability Memory loss Focal neurological deficits such as limb weakness or spasticity
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contraindications to LP
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
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USS giant cell/temporal arteritis
halo sign
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features of carbon monoxide posioning
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
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invetsigation CO posioning
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
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Management CO poisoning
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

Core clinical problems (94 decks)

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