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RLH MRCS > DrE: Neuro > Flashcards

DrE: Neuro Flashcards

1
Q

What is AMTS?

A

Abbreviated mental test score

Screening question of 10 questions

<6/10 = dementia/delirium & should precipitate mini-mental state examination

  1. How old are you?
  2. What is the time (to the nearest hour)?
  3. Can you remember an address? - I will ask you again at the end
  4. What is the year?
  5. What is the name of the hopsital where the patient is?
  6. Can you identify 2 people - doctor/nurse/family member ?
  7. What is your DoB ?
  8. What date did WW2 begin/end? 1939/45
  9. Who is the current prime minister/monarch/president?
  10. Can you count backwards from 20
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2
Q

What is a MMS?

A

Mini Mental State Examination

Should be performed on all patients who achieve an AMTS <6/10

24-30 = no cognitive impairment / 18-23 mild / 0-17 = severe

  • Orientation:
    • What is the year/season/date/month/day of the week (/5)
    • What is the country/region/city/hospital/ward (/5)
  • Registration:
    • Remember 3 items clearly names e.g. pen book shoe, repeat back - count number of trials required (/3)
  • Attention/calculation:
    • count back from 100 in 7s 5 times (up to 65) OR spell WORLD backwards (/5)
  • Recall
    • recall 3 items from earlier (/3)
  • Language & praxis
    • name 2 objects e.g. pen, watch (/2)
    • Repeat the phrase ‘no ifs, ands or buts’ (/1)
    • take a piece of paper in your right hand, fold it in half, put it on the table (/3)
    • wrist the following on a piece of paper: ‘close your eyes’ and instruct the patient to follow the command written (/1)
    • Instruct the patient to make up a complete sentence and write it on a piece of paper (/1)
    • ask patient to coppy a picture (2 hexagons overlapping) (/1)

/30

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3
Q

How to perform GCS?

A

Patient ideally sitting out in chair

ask patient if they are in pain

ask patient if they are on any medications that may influence their GCS

Eyes /4

4- open spontaneously

3-open in response to speech

2-open in response to pain

1-no response

Voice /5

5- orientated (child: smiles, orientated to sounds, follows objects, interacts)

4- confused (child: cries but consolable, inappropriate interactions)

3- inappropriate speech i.e. words (child: inconsistently consolable, moaning)

2-incomprehensible sounds (child: inconsolable, agitated)

1- no response (child: no response)

Motor /6

6- obeys commands

5- localises to pain

4- flexion withdrawal

3- abnormal flexion to pain (decorticate)

2-abdnormal extension to pain (decerebrate)

1- no response

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4
Q

Limitations to GCS

A
  • GCS is reproducible, objective assessment of patient’s conscious level
  • Assessment in young children can be difficult - use of modified verbal scoring system
  • GCS = to 8 = coma & warrants intubation
  • Beware of language barriers may appear to inhibit the patient’s response
  • Other trauma may prevent following commands e.g. spinal injury
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5
Q

Disorders of speach to note at start of CN examination?

A
  • Dysarthria: Disorder of articulation Caused by ETOH/Cerebellar disease/Head injury/lesions to V/VII/IX/X/XII
  • Dysphonia: Disorder of phonation due to vocal cord impairment e..g. vocal cords
  • Dysphasia: Disorder of language - expressive, receptive, mixed
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6
Q

What is dyskinesia?

A

Disorder of movement characterised by involuntary muscle movements

  • Fasciculations - small involuntary muscular contractions
  • Tremor - involuntary & rhythmical oscillatory muscle movements
  • Dystonia - sustained involvuntary muscle contractions, resulting in twisting & repetitive movements or abnormal postures
  • Chorea - rapid involuntary jerky movements that may be highly variable in location
  • Tic - rapid involuntary sudden movements that are stereotypical in location
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7
Q

How to examine Optic nerve?

A

AFRO

  • Acuity:
    • Snellen chart - without then with vision aids e.g. 6/6 (distance from chart)/(line on chart):
      • Closer
      • Fingers held up
      • Hand movements
      • Light
      • No Perception of Light NPL
  • Colour: Ishihara plates
  • Fields:
    • Confrontation
    • Red hat pin for scotomas (colour vision fails early in optic nerve & retinal disorders)
      • a partial loss of vision or blind spot in an otherwise normal visual field
  • Reflexes/Pupils:
    • Size & symmetry
    • Direct & consensual
    • Accomodation
    • Swinging light reflex - light shines on affected eye and it continues to dilate slightly = Marcus Gunn Pupil - optic nerve injury/MS
  • Optic disc/Fundoscopy:
    • red reflex
    • Disc - colour, contour, cupping
    • Disc margins/lack of retinal venous pulsations
    • Macula - look straight into the light
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8
Q

How to examine eye movements?

A

III - oculomotor, IV Trochlear, VI Abducence

H manouevre

Most = occulomotor = III

SOiv Superior oblique mucles = trochlear = IV = adducts the eye with inferior gaze

LRvi Lateral recturs = abducence = VI = abducts the eye

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9
Q

How to examine trigeminal nerve?

A
  • Sensort:
    • fine touch - cotton wool of ophthlamic Vi/Maxillary Vii/Mandibular Viii
    • Corneal reflex (sesation Vii, motor VII)
  • Motor:
    • Open mouth - if unilateral lesion affecting pterigoid, jaw deviates TOWARDS side of lesions
    • Jaw Jerk - finger on mandible & tap with T hammer, +ve -> masseter +ve & jaw closure = UMN lesion (pure V)
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10
Q

How to examine Facial nerve VII?

A
  • Facial asymmetry - on inspection
  • Sensorr:
    • Chorda tympani - Change in tast on ant 2/3 tongue (post 3rd IX)
    • Motor:
      • raise eyebrows, screw eyes, blow out cheek, show teeth, tense/flare neck muscles
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11
Q

How to examine Vestibulocochlear nerve VIII?

A
  • whisper in each ear
  • Rinne’s test - tuning fork 512 - on mastoid process, then lat to ear.
    • Normal = detects sound again once lat to ear
    • Conductive hearing loss = unable to detect sound again
  • Weber’s test - tuning fork 512 - on forehead
    • normal = equal
    • Conductive = louder in affected ear
    • Sensorineural = lounder in unaffected/normal ear
  • Vestibular function
    • Oculocephalic reflex in comatosed patient
      • flex neck & quickly rotate side to side - eyes move left when head moved right = doll’s eyes
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12
Q

How to examine glossopharyngeal/vagus nerve (IX/X)?

A
  • Gag reflex
  • X = uvula deviates away from affected side
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13
Q

How to examine Spinal accessory (XI)?

A
  • shrug shoulders against resistance (trapezius)
  • turn head to side against resistance (SCM - laterally rotates head to contralateral side)
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14
Q

How to examine hypoglossal XII?

A
  • protrude the tongue, asssess symmetry, wasting, fasciculations
  • Tongue deviates towards side of lesion
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15
Q

What to assess on general inspection for a Peripheral Nervous System Examination?

A
  • Gaite
  • Spine - kyphosis, lordosis, scoliosis
  • Fasciluations
  • Romber’s - loss of proprioception
  • Cerebellar signs: DANISH:
    • Dysdiadokinesia
    • Ataxia
    • Nystagmus
    • Intention tremor & past pointing
    • Slurred speach
    • Hypotonia
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16
Q

Upper limb power examinaition:

which never root/movement/muscle/nerve

A
  • C5 - shoulder abduction - deltoid - axillary
  • C5/6 - elbow flexion - biceps/brachioradialis - musculocutaneous/radial
  • C7/8 - elbow extension - triceps - radial
  • C7 - MCPJ extension - Extensor digitorum communis - posterior interosseous (radial)
  • C8 - Thumb IPJ Flexion - Flexor policis longus - anterior interosseous (median)
  • T1 - Finger abduction - dorsal interossei - Ulnar
  • T1 - Thumb Abduction - abductor policis brevis - median
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17
Q

Lower limb power examinaition:

which never root/movement/muscle/nerve

A
  • L2/3 - hip adduction - hip adductors - obturator nerve
    • gracilis, obturator externus, adductor brevis, adductor longus and adductor magnus
  • L2/3 - hip flexion - illiopsoas - femoral nerve
  • L4/5- hip extension - gluteus maximus - sciatic
  • L3/4 - knee extension - quadriceps - femoral nerve
  • L5/S1 - Knee flexion - hamstrings - sciatic nerve
    • biceps femoris, semitendinosus, and semimembranosus
  • L4/5- ankle dorsiflexion - tibialis anterior - deep peroneal
  • S1/2-ankle plantarflexion - gastrocnemius - tibial
  • L5 - Hallux extension - Extensor hallicus longus - deep peroneal
  • L5/S1 - ankle eversion -peronei - superficial peroneal
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18
Q

UK MRC Power grading

A
  • O = no movement
  • 1 = contraction flicker
  • 2= movement without gravity
  • 3= movement against gravity
  • 4= movement against resistanct
  • 5=full power
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19
Q

Different sensation tracts

A
  • Spinothalamic:
    • pain
    • temperature
  • Dorsal column:
    • Light touch
    • Proprioception
    • 2 point discrimination
    • vibratino
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20
Q

Reflexes and corresponding arc

A
  • Ankle - S1/2
  • Knee - L3/4
  • Biceps - C5/6
  • Supinator - C5/6
  • Triceps - C7/8
  • Babinski - L4-S2
  • Abdominal - L7-T12
  • Cremasteric - L1/2
  • Anal - S2-4
  • Bulbocavernosus - S2-4
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21
Q

Grading reflexes

A
  • 0=absent
  • +/- = present with reinforcement
    • hyporeflexia
  • ++ normal
  • +++hyperreflexia
  • ++++hyperreflexia & clonus
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22
Q

What is the epidemiology of low back pain?

A
  • Life time incidence >85%
  • Most common reason for disability age <45y
  • No sig race/sex difference
  • increases with age/pregnancy
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23
Q

Common causes of lower back pain?

A
  • Congenital - scoliosis/kyphosis/spina bifida/spondylolisthesis
  • Degenerative - OA/Spondylosis/Facet joint hypertrophy
  • Metabolic - osteopersosis
  • Infective - osteomyelitis/TB/Discitis
  • Inflammatory - Ankylosing spondylitis
  • Musculoskeletal - posture related muscle spasm (commonly lumbar)
  • Neurological - spinal canal stenosis, prolapsed intervertebral disc, spinal haematoma
  • Psychological - Functional overlay
  • Traumatic - vertebral fractures, muscle tears, ligamentous injuries
  • Neoplastic - primary (uncommon) secondary (more common)
  • Renal - calculi, renal cell carcinoma
  • Gynaecological - endometriosis/pelivic inflammatory disease/tumours
  • Vascular - AAA
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24
Q

What is the mechanism of a prolapsed intervertebral disc?

A
  • Posterior herniation, of central nucleus pulposis, through annular fibrosis, into spinal canal
  • 50% = L4/5, 40% L5/S1
  • Caused by degenerative cascade:
    • dysfunction - acute inj, tear annulus fibrosis & prolapse of inner NP with cartilage destruction. Inflmmatory facet joint reaction
      • back pain - worse on movement, with localised tenderness on palpation, muscle spasm. Significant prolapse -> impinge nerve root -> radiculopathy/cause equina
    • instability - disc resorption, loss of height. Facet joins lax, predispose to sublucation
      • intermitent back pain, possible detectable instability on movement. neurological deficit persists/worsens
    • restabilisation - osteophyte formation, progressive stenosis
      • chronic back pain, reduced severity, neurological deficits stabilise
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25
Q

What investigations would aid Dx of prolapsed IV disc?

A
  • MRI = gold standard
    • urgent if cause equina syndrome suspected
  • CT (myelogram) = if MRI contraindicated/unavailable
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26
Q

What are the clinical features of lumbar radiculopathy secondary to prolapsed intervertebral disc?

A
  • L4/5 -> compression of ipsilateral L5 nerve root
    • L5 dermatome pain & sensory impairment
    • Weak foot porsiflexion
    • Weak extensor hallicus longus
  • L5/S1 -> compression of ipsilateral S1 nerve root
    • S1 dermatome pain & sensory impairment
    • weak foot plantarflexion
    • depressed/absent ankle jerk
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27
Q

What are the treatment options for lumbar radiculopathy, secondary to prolapsed intervertebral disc?

A
  • Conservative:
    • Lifestyle modification & patient education
    • OT/PT
    • Heat/Hydrotherapy
    • TENS machine
  • Medical:
    • Analgesic ladder
    • Epidural/nerve root injections
  • Surgical: <20%, indicated by cauda equina syndrome, intractable pain, progressive motor deficit (Grd= to 3)
    • Lumbar discectomy:
      • >90% improvement & 5% recurrence rate
    • Lumbar discectomy & laminectomy - for canal stenosis
    • Lumbar arthrodesis - for spondylosis
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28
Q

What is cauda equina syndrome and what are the characteristic features?

A
  • results from compression of cauda equina nerve roots (L2-5 + S1-5+ Coccygeal)
  • secondary to prolapsed intervertebral disc (commonly)
  • constitutes surgical emergency
  • Also caused by :
    • heamatoma
    • infection
    • inflammatory conditions
    • malignancy
    • trauma
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29
Q

What are the characteristic features of cauda equina syndrome?

A
  • Red flags:
    • Severe lower back pain
    • Bilateral sciatica
    • Saddle anaesthesia & genital sensory deficit
    • Bowel and bladder sphincter dysfunction
    • Sexual dysfunction
  • 3 typical presentations:
    • Sudden onset
    • Acute bladder/bowel dysfunction - in a patient with lower back pain & sciatica
    • Gradual progression
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30
Q

How would you classify cauda equina syndrome?

A
  • Incomplete:
    • Difficulty urinating
    • altered sensation on defecating
    • unilateral/partial perianal & genital sensory deficit
    • residual anal tone
  • Complete:
    • painless urinary retention +/- overflow
    • Altered/no sensation on defecating
    • Bilateral perianal and genital sensory deficit
    • Absent anal tone
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31
Q

What questions are important to ask in history and what examination features are essential to document in cauda equina syndrome?

A
  • History:
    • Do you have pain in both legs? is it worse than the back pain?
    • When did you last pass urine/open your bowels?
    • Do you have difficulty urinating - is there dribbling/leakage?
    • Can you feel the paper when you whipe your bottom?
    • Do you have numbness in your bottom & genitals?
  • Examination:
    • assess and document genital sensation
    • assess and document perianal sensation and anal sphincter tone (per rectum examination?
    • On catheteridation, document residual urine and catheter tug sensation
    • Document lower limb tone, power, coordincation, reflexes
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32
Q

What are the treatment options for cauda equina syndrome caused by disc prolapse?

A
  • neurosurgical emergency
  • irreversible ischaemia occurs at c.6hrs
  • surgical decompression is via discectomy & decompressive laminectomy - of 1-2 vertebrae
  • incomplete cauda equina syndrome = good prognosis if surgery <12hrs of onset
  • Complete cauda equina sndrome = limitted prognosis - recovery is <24hrs of onset
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33
Q

What is the epidemiology of head injuries?

A

estimared 1mil ED attendances/yr

200,000 hopsital admissions

4,000 undergo neurosurgery/yr

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34
Q

Important Qs for history taking in a patient with a head injury?

A
  • Mechanism - assault/falls/RTA. If fall - precipirating syncopal event?
  • loss of conciousness - duration? witnessed? 3rd party history where possible
  • Amnesia
    • Retrograde: unable to recall events prior to injury
    • Anterograd: unable to recall events after injury
  • Raised ICP symptoms: headache, nausea, vomiting, visual disturbances, focal neurological deficit
  • General: medical and surgical co-morbidities, medications e.g. anticoagulants/antiplatelets, allergies, last meal
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35
Q

What signs would you look for to confirm a head injury?

A
  • External trauma: ecchymoses, lacerations, haemorrhage
  • Base of skull fracture: periorbital bruising (panda/raccoon eyes), retroauricular bruising (battle sign), CSF ottohorea/rhinorrhoea, bleeding from ear/behind tympanic membrane
  • GCS: at scene & post resusc, GCS = to 8 = INTUBATE
  • Pupils: asymmetry, reaction to light
  • Focal Neurological Deficit: CN palsy, limb motor weakness, sensory deficit
  • Associated Spinal trauma: bruising, vertebral fractures, poor anal sphincter tone (PR)
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36
Q

When would you request a CT brain (& cervical spine) after a head injury?

A
  • Immediate CT brain:
    • ABSOLUTE:
      • GCS <13 on initial assessment in ED
      • GCS <15 more than 2hrs post injury
      • Suspected open, depressed, base of skull #
      • Post traumatic seizure
      • Focal neurological deficit
      • >/= 2 episodes of vomitting (>/=3 in children)
      • Amnesia of events >30 minutes pre-impact
    • CONSIDER if high risk criteria:
      • >65yo
      • coagulopathy
      • Dangerous MOI e.g. ejection from vehicle, pedestrian V vehicle
  • CT cervical spine (in addition to brain)
    • GCS <13 on initial assessment in ED
    • Intubated
    • Suspected abn on plain film/technically inadequate film
    • Scanned for multiregional trauma
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37
Q

How would you classify the sevetiry of head injury?

A
  • Open e.g. stabbing/gunshot/compound fractures
  • Closed e.g. blunt trauma
  • GCS:
    • 14-15 = minor (80%)
    • 9-13 = moderate (10%)
    • # to 8 = severe (10%)
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38
Q

When would you refer a patient with a head injury to a neurosurgeon?

A

ALL moderate/severe head injuries

  • New ‘surgically significant’ abnormality on CT
  • GCS = 8 persisting after resuscitation
  • Unexplained confusion >4hrs
  • Deterioration in GCS (by >/= 2 points)
  • Progressive focal neurological deficit
  • Seizure without full recovery
  • Open or suspected open injury
  • CSF leak
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39
Q

What are the principle of management of a minor head injury in a non-neuroscience centre?

A
  • Manage according to ATLS resuscitation principles
  • GCS = 15, obs incl RR/HR/BP/SpO2/GCS /Pupils/functional neurological deficit:
    • 1/2 hrly for 2 hrs
    • hrly for 4 hrs
    • 2 hrly thereafter
  • Adequate analgesia (caution with opitates)
  • Adequate hydration & check electrolytes incl Na
  • Consider anti-epileptics (discuss with neurosurgeons)
  • Consider rescan & rediscussion with neurosurgeon if GCS deteriorates, worsening headache, nausea, vomiting
  • Consider referral to neurorehabilitation for post concussional syndrome
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40
Q

Indications for emergency neurosurgery following head injury?

A
  • Extradural/subdural haematoma with >5mm midline shift
  • Intra-cerebral haematoma >40mm^3 in surgically accessible area
  • Depressed skyll fracture with depression > skull thickness
  • Potentially all open injuries - wound exploration - no role for prophylactic ABx in base of skull #
41
Q

What are the management principles for severe head injuries that do not require immediate neurosurgery?

A
  • Primary:
    • Prevent secondary brain injuryy, cerebral ischeamia, herniation
      • increasing ICP => reducing CPP => reducing O2 supply + CO2 clearance => ischaemia and vasodilation
        • vicious cycle

ATLS

Intubation and ventilation in ICU

Insertion of ICP monitor

Optimise potential for recovery using medical and surgical strategies to maintain:

  • CPP >65
  • ICP <25
42
Q

Stepwise management of head injury to prevent secondary brain injury…

A
  • Teir 1:
    • Elevate head (30-45)
    • Avoid hypoxia & hypercapnoea
    • Sedate and paralyse: decrease O2 demand and cerebral blood flow -> decrease ICP
    • Control PaCO2 (4-4.5kPa): Moderate hyderventilation ‘blows off’ CO2 to help prevent cerebral vasodilation
    • Maintain MAP: maintain CPP
    • Ensure Normothermia
    • ?Surgical:
      • External ventricular drainage: therapeutic CSF withdrawal to control ICP
  • Teir 2 (Teir 1+…)
    • Increase sedation: boluses if req
    • Induce hypothermia (33-35): reduce metabolic demand
    • Manitol (osmotic diuretic)/Hypertonic saline (target Na 145-155): reduce cerebral oedema. Risk of renal impairment when serum osmol >320mOsm/Kg water
    • Surgical:
      • External ventricular dainage: therapeutic CSF withdrawal to control ICP
  • Teir 3 (Teir 1 + 2 + …)
    • Barbiturate coma (e.g. thioentone) induced ‘total cerebral narcosis’ & reduces brain metabolic demand to minimum requirement. Risks incl myocardial depression, hepatic & renal impairment
    • Surgical:
      • External ventricular drainage
        • decompressive craniotomy - alows cerebral herniation through the defect
43
Q

What are the possible neurological sequelae for survivors of severe head injury?

A
  • Vegetative state: no physical recovery
  • Cognitive impairment: concentration and memor impairment
  • Epilepsy: partial/general seizures
  • Location specific:
    • Brainstem - locked in syndrome
    • Frontal - disinhibition, emotional disturbance, personality disorder
    • Temportal - aphasia
    • Motor cortex - mono- hemi- tetraperesis
  • Psychiatric: delirium, depression, psychosis
44
Q

What are the most common causes of intracranial haemorrhage?

A
  • Trauma - most common
  • Spontaneous intracerebral haemorrhage - haemorrhagic stroke
  • Subarachnoid haemorrhage
45
Q

Mechanism and features of an extra-dural haemorrage?

A
  • High pressure arterial origin (middle meningeal artery most commonl)
  • >85% assoc with skull ‘
  • Decreased GCS & contralateral side hemiparesis is common
  • <30%: ‘Talk and die’
    • LOC -> Lucid interval -> Rapid deterioration
  • Variable underlying brain injury
  • High density biconvex lesion on non-contrast CT scan aka lentiform
46
Q

Mechanism and features of s sub-dural haemorrage?

A
  • Venous origin
  • Cortical laceration in young - often with significant underlying brain injury
  • Bridging veins between inner table of skull and brain in elderly
  • Decreased GCS & contralateral hemiparesis = common
  • High density, concave lesion on non-contrast CT scan - semilunar
47
Q

Mechanism and features of an intracerebral haemorrage/Contusion?

A
  • Direct brain injury
  • Inferior frontal lobe and temporal lobe due to anatomy of skull base c.85%
  • Decreased GCS & focal neurological deficit is characteristic
  • Symptoms may worsen after 24-48hrs
  • High density lesion in affected area on CT scan, with surrounding low density cytotoxic oedema
  • Coup = direct injury
  • Countrecoup = injury on opposite side of direct injury
48
Q

Management options for traumatic EDH?

A

​ATLS resuscitation and head injury principles +

  • Conservative - if small
  • Endovascular embolisation - if small
  • Craniotomy & evacuation:
    • if increasing size/>0.5cm thick with >5mm midline shift / deteriorating GCS
49
Q

Management options for traumatic SDH?

A

ATLS resuscitation

head injury principles +

  • Conservative - if chronic/small
  • Trial of steroids - if chronic
  • Burr hole drainage - if chronic with mass effect
  • Craniotomy & evacuation - if >1cm thick with midline shift/focal neurological deficit/deteriorating GCS
50
Q

Management options for traumatic ICH?

A

ATLS resuscitation

Head injury principles

  • conservative - mostly
  • Craniotomy & evaculation - if >40mm^3 or with inferior temporal lobe/cerebellum incolvement sure to risk of brainstem compression
  • Bifrontal decompressive craniectomy - for small/diffuse bifrontal contusions with mass effect

note with ICH delayed deterioration is common due to maturation of contusion, peaking at 3-6 days

51
Q
A

Extradural (+extracranial scalp haematoma)

52
Q
A

Subdural haematoma (&midline shift)

53
Q

What is the difference between intracranial and subarachnoid haemorrhage?

A

ICH - haemorrhage into brain parenchyma (intra-axial)

SAH - haemorrhage into subarachnoid space (extra-axial)

54
Q

What are the risk factors for spontaneous intracerebral haemorrhage?

A

10-15/100,000, >80% secondary to HTN & amyloidosis

Risk factors:

  • Unavoidable:
    • Age >55yrs
    • Race Afro-caribbean>caucasian
  • Iatrogranic
    • Post operative (especially malignant tumours)
  • Medical:
    • Coagulopathy (hepatic failure/anticoagulation)
    • HTN (affects basal ganglia & brainstem)
    • Amyloidosis (amyloid angiopathy weakens blood vessel walls)
  • Vascular:
    • Aneurysm
    • AVM
  • Social:
    • illicit drugs - most common cause in <30s (amphetamines, cocaine)
55
Q

What are the tratment principles of spontaneous intracerebral haemorrhage?

A
  • Conservative:
    • modify RF
  • Medical:
    • Resuscitation
    • Control HTN
    • Reverse anticoagulation
  • Surgical
    • Craniotomy and evacuation

Current evidence base overall does not support surgical intervention. In general right hemisphere peripheral parietal haematomas are most favourable for surgery. Basal ganglia & brainstem haematomas are least favourable

56
Q

What is the epidemiology of SAH?

A
  • Annual incidence 10-15 per 100,000
  • increased prevalence in patients 50-65
  • F:M 1.5:1
  • Afro caribbean:caucasian 2:1

Note - prevalence of intracranial aneurysms = 4-7%, most do not rupture & remain asymptomatic

57
Q

What are the causes of SAH?

A

80% are due to ruptured aneurysm, 15% have multiple aneurysms

  • Idiopathic: no identified cause
  • Aneurysm:
    • berry aneurysm (saccular) rupture, >75%
    • Infective e.g. endocarditis
    • Inflammatory
  • Arteriovenous malformation:
    • AVM
    • Dural arteriovenous fistula - acquired
  • Trauma: uncommon & usually with different radiological distribution of blood v spontaneous bleeds
58
Q

What features on Hx and Ex suggest SAH?

A

consider in any patient presenting with sudden onset, severe headache

5-10% die immediately, 15% commatosed on arrival in ED

  • History:
    • Very sudder, max intensity <1min
    • Persisting
    • Worst ever experienced
    • Variable location - classically occipital
    • Dull/boring character
    • Assoc
      • nausea & vomiting
      • LoC
      • Seizure
  • Examination:
    • Normal
    • Meningism
    • Focal neurological deficit
    • Visual defect - ophthalmic artery aneurysm
    • Papilloedema - uncommon acutely as develops >6hrs from onset
    • drowsiness
    • coma
59
Q

What investigations would you order to confirm SAH?

A
  • CT brain (non-contrast): sensitivity >96% in 1st 6 hrs, drops to 80% at 3 days, superior to MRI
  • LP: if CT normal, perform at >12hrs, sensitivity drops but can perform up to 14 days, CSF bili indicates SAH, raised oxyhaemoglobulin -> false negative bili result, obtain CSF WCC, RBC count, protein, oxyhaemoglobin, bili absorbance ratios
60
Q

What imaging would you obtain to detect an intra-cranial aneurysm?

A
  • CT angiogram - detects most aneurysms except smallest
  • MR angiogram - better detection at skull base than CT
  • Catheter angiogram - gold standard but invasive and carries 1/1000 risk of stroke
61
Q

What are the treatment options for a proven aneurysmal SAH?

A

Aim: secure the aneurysm and reduce the risk of rebleeding:

  • conservative: supportive - considered in pt with poor recovery from initial SAH, elderly pt, pt with sig comorbidities
  • Interventional: endovascular embolisation with colis (for >80% of pt with aneurysms in uk, only 50% in USA). procedure involves femoral catheterisation, passage of microcatheters to the cerebral vasculature & deployment of coils into aneurysm sac. Most suitable for aneurysms with large dome & narrow neck. some require stent assistance to assist access
  • Surgical: craniotomy & titanium clipping of aneurysm neck (prevents aneurysm filling) performed when coiling has failed/is technically unfeasible OR an existing requirement for craniotomy e.g. evacuation of large heamatoma due to SAH
62
Q

What is a stroke?

A

clinical syndrome, with underlying vascular cause, of rapidly developing clinical features of focal or global disturbance in cerebral function lasting >24hrs or leading to death

63
Q

what is a TIA

A

Like a stroke but clinical features last <24hrs

64
Q

What is the epidemiology of a CVA?

A
  • 3rd most common cause of death in developed countries
  • affects 200 per 100000 people per year
  • commonly in 65-75 yr age group
  • significant cause of morbidity in aging pop
65
Q

What is the pathophysiology of a stroke?

A
  • CVA may be haemorrhagic (spontaneous ICH), thrombotic or embolic
  • Thrombotic are due to atherosclerosis resulting in atheroma formation within the affected blood vessel and subsequent acute occlusion
  • embolic CVAs most common originate from a site of thrombus e.g. at the carotid artery bifurcation/from the cardiac atria in AF. Other emboli include fat, air and FB
  • the result of the above is brain parenchyma damage
66
Q

What are the risk factors for a stroke?

A
  • Non-modifiable:
    • age
    • gender M>F
    • Diabetes
    • genetic predisposition
    • essential medications e.g. warfarin - haemorrhhagic stroke
  • mobifiable:
    • HTN
    • Hypercholesterolaemia
    • Obesity
    • Poor diet
    • smoking, ETOH, sedentary lifestyle, stress
67
Q

What is the management strategies for stroke?

A

Hospital admission for thorough investigation and diagnosis (CT/angio)

Treatment

  • prevention:
    • reduced risk factors
    • treat predisposing conditions
  • medical:
    • anticoagulant
    • thrombolysis
    • calcium antagonists e.g. nimodipine
    • aspirin
    • good INR control (if on warfarin)
  • Surgical:
    • carotid endartectomy
    • Superficial temporal to middle cerebral artery anastomosis

Risk factor identification and reduction - stroke unit

Rehabilitation - PT/OT

Care plan implementation - DN/care home

psychological support

68
Q

What is hydrocephalus?

A

It is an imbalance between CSF production and absorption, usually due to increased CSF volume and pressure

May cause increased ICP, progressive head enlargement, convulsions, mental disability, coma, death

69
Q

What do you know about CSF production?

A

average adult ventricular system contains 150ml CSF

CSF is produced by the choroid plexus and ependyma at 20ml/hr (480ml/day)

CSF is reabsorbed by the arachnoid villi

70
Q

How would you classify hydrocephalus?

A
  • Increased CSF production
    • choroid plexus papilloma
    • Choroid plexus carcinoma
  • Impaired CSF circulation
    • obstructive - impairment within ventricular system. ventricles DO NOT communicate with subarachnoid space
      • congenital aquaduct stenosis (obstructs aqueduct of sylvius)
      • Congenital arnold-chiari malformation (obstruction and foramen magnum)
      • Thalamic tumour - obstructs 3rd ventricle
      • Cerebellar tumour - obstructs 4th ventricle
    • communicating - impairment within subarachnoid space. ventricles DO communicate with subarachnoid space
      • head injury
      • infection - brain abscess/meningitis
      • SAH
  • Impaire absorption:
    • sinus thrombosis
    • SAH
    • Superior vena cava syndrome
  • Other:
    • benign intracranial HTN
    • Normal Pressure Hydrocephalus
71
Q

How does hydrocephaolus present

A

depends on several factors incl age, speed and duration of onset, cause

clinical features:

  • acute (hrs-days)
    • infant - poor feeding, drowsiness/irritability, bulging anterior frontanelle, sunsetting eyes (downward gaze and lid retractions = parinaud’s syndrome), distended scalp veins, increasing head circumference
    • adults - severe headache, nausea & vomiting, visual disturbance, gait disturbance, focal neurological deficit, papilloedema, drowsiness, coma
  • subacute (days-weeks)
    • more insidious onset with morning headaches, nauea and vomiting, upward gaze failure, delayed deterioration after initial recovery
  • Chronic (months)
    • cognitive impairment, gait disturbance, bowel incontinence, neck pain
72
Q

What imaging would you request for hydrocephalus?

A

full Hx and examination followed by

  • USS - useful in infants (via anterior frontanelle)
  • CT - reveals ventricular size and configuration
  • MRI - reveals small SOL missed on CT and other assoc brain abn
73
Q

Treatment options for hydrocephalus

A
  • medical:
    • acetazolamide, furosemide - reduces CSF secretion (ineffective in long term)
    • isosorbide - increases CSF absorption (ineffective in long term)
  • Interventional
    • serial anterior fontanelle CSF taps in infants
    • serior LP in adults up to 2x/day
      • useful in pt with transient communicating hydrocephalus e.g. post SAH, not practical in LT but avoids surgery
  • Surgical
    • Ventriculoperitoneal shunt - most useful, extends forom right lateral ventricle (in right parietal region) to the peritoneum, prone to blockage c.50% <2 yrs, tubing fracture and infection
      • very effective!
    • Ventriculoatrial shunt - extends from right lateral ventricle to jugular vein. Used when abdomen not suitable e.g. peritonitis/multiple abdo surgeries. rare assoc with glomerulonephritis
      • very effective!
    • Endoscopic 3rd ventriculostomy - endoscopic fenestration of 3rd ventricle floor creating new CSF flow channels. Most efficacious in adults with obstructive hydrocephalus.
      • Less effective than shunts
    • Ventriculopleural shunt - last resort when abdo/cardiac shunts are not suitable. Pleural effusion is a common complication
      • very effective!
    • Lumbar peritoneal shunt - benign intracranial HTN and some types of communicating hydrocephalus
      • very effective in selected cases
74
Q

What are the most common CNS infections?

A

Infection - viral, bacterial, fungal, parasitic

Divided - cranial & spinal

Cranial:

  • Brain abscess:
    • staph aureus
    • strep milleri
    • Bacteroides spp
    • Pseudamonas aeruginosa
  • Subdural emyema:
    • streptococcus milleri >60%
    • haemophilus spp
    • anaerobes
  • Meningitis:
    • neonates:
      • group B/D strep
      • escherichia coli
      • staph aureus
    • Infant/young child
      • neisseia meningitidis
      • strep penumoniae
      • Haemophilus influenzae
    • Teenager/adult
      • neisseria meningitidis
      • strep pneumoniae
    • trauma/post op
      • staph aureus
      • pseudomonas spp
      • enterobracter spp
      • mycobacterium tuberculosis
  • Ventriculitis
    • coagulase ive staph
    • escherichia coli

Spinal

  • prumary discitis
    • staph epidermidis
    • staph aureus
    • escherichia coli
    • proteus spp
    • pseudomonas spp (common in IVDU)
75
Q

Subdural empyema

A

pus rapidly spreads along the subdural space but does not cross boundaries e.g. falx cerebri & tentorium cerebellum

Cause: iatrogenic e.g. post op, spread of pus from sinusiti, otitis media, mastoiditis

Features: fever, lethargy, reduced consiousness, focal neurological deficit, seizures in 70% cases

Investigations: diagnosis difficult even with CT

Treatment: as per brain abscess

76
Q

Meningitis

A

Inflammation of the meninges of the drain and spinal cord

Cause: infection, iatrogenic (post op), chemical (intrathecal drugs), tumour (brain tumour/lymphoma), inflammatory sarcoidosis, traumatic (penetrating head injury, base of skull fracture

Features: meningism, decreased GCS, focal neurological deficit, sepsis (petechial rash in meningococcal spesis)

Investigations: bloods (FBC, U&E, CRP, cultures)

CT brain (excludes mass lesion)

LP (mircrobiology-gram stain, MC&S/biochem - protein glucose, WCC/virology * immunology as required)

Treatment: resuscitation, broad spec ABx immediately (gram neg cover), analgesia, possibly corticosteroids, definitive management depends on cause

77
Q

Ventriculitis

A

Inflammation of the ventricular cavity & ependymal lining

Cause: VP shunt, intrathecal chemotherapy, post meningitis (rarely aseptic)

Features: decreased GCS, sepsis, enhacing ventricles on imaging

Investigations: LP (CSF sample establishes diagnosis)

Treatment: intrathecal & intravenous antibiotics until CSF clear, remove shunt, re-site EVd

78
Q

Primary discitis

A

Infection of nucleus pulposus, then vertebral body

Cause: iatrogenic e.g. post op (0.2-4% incidence after lumbar discectomy) immunocompromise e.g. HIV, IVDU, DM, Obesity, multiple surgeries, sepsis at time of op = risk factors

Feaures: severe localised pain worse on spinal movements, radicular symptoms, tenderness, muscle spasm

Ix: blood tests e.g. XR normally in 1st week

Treatment: brace, bed rest, analgesia, ABx (4-8 wks), surgery (for assoc abscess/unstable spine)

79
Q

What factors pre-dispose to brain abscess development?

A
  • Contiguous spread - from ENT infection into adj brain:
    • sinusitis -> inferior frontal lobe / Mastoiditis -> inferior temportal lobe
  • Head injury - penetrating head injury
  • Immunocompromise - HIV, steroids, DM
  • Systemic - bacterial endocarditis, congenital cyanotic heart disease
80
Q

What are the common clinical features of brain abscesses?

A

Most patients present with a history of symptoms <2 wks:

  • headache - 70%
  • Mental state changes 65%
  • Focal neurological deficit 65%
  • Fever = 50%
  • N&V = 40%
  • Seizures = 30%
  • Nuchal rigidity = 35%
  • Papilloedema = 25%
81
Q

What are the treatment options for brain abscesses?

A
  • Medical:
    • empirical ABx -> specific (with MC&S) +/- intrathecal antibiotics (for intraventricular extension
    • Anticonvulsants >6mo
  • Surgical:
    • Image guided burr hole & abscess aspiration (repeat if necessary)
    • Craniotomy and surgical excision
    • Ventricular drainage (for intraventricular extension)
  • Follow up
    • clinical progress
    • Serial imaging
    • Serial inflammatory markers
82
Q

What are the causes of an intracranial mass lesion?

A
  • Congenital: arachnoid cyst, hamartoma, dermoid cyst
  • Infection: abscess, toxoplasmosis, subdural empyema, hydatic cyst
  • Inflammatory: MS, reactive around FB
  • Neoplastic: primary & secondary tumours
  • Trauma: extradural heamatoma, subdural heamatoma, intracerebral haematoma
  • Vascular: aneurysm, AVM, carvernoma
83
Q

What is the epidemiology of brain tumours?

A
  • Primary brain tumours - annual incidence of 7.5/100,000 & >3,500 deaths/yr
  • 15th most common cancer in adults & 2nd most common in children after leukaemia
  • Metastases acct for 50% of brain Tx & prevalence increases with age
  • Mets are found in c.25% of post mortems (with brain Ex)
  • Despite modern Rx, primary Tx depend on primary pathology & extent of metastatic spread
84
Q

What RF are assoc with development of brain Tx?

A

Most arise in pt without obvious predisposing factor

<5% assoc with genetic conditions incl von recklinghausen’s disease (NF1), tuberous sclerosis (TSC1 &2) Li Fraumeni syndrome (P53)

Radiation exposure e.g. previous whole brain radiotherapy

Immunocompromise e.g. HIV, primary CNS lymphoma

Possible increased risk from certain chemical exposures

No proven link with mobilse phone use or previous head injury

85
Q

How would you classify brain tumours?

A
  • Primary (45%):
    • Intra-axial:
      • Glioma (69%):
        • Astrocytoma (61.5%)
        • Oligodendroglioma (5%)
        • Ependymoma (2.5%)
      • Lymphatic (3%):
        • Lymphoma
    • Extra-axial:
      • Meningioma (20%)
      • Pituitary (5%)
      • Cerebellopontine (3%)
  • Secondary:
    • metastases:
      • lung (60%) - small cell carcinoma
      • Breast (20%) - oestrogen receptor positivity predicts favourable response to chemotherapy
      • Others (20%): colon, melanoma, prostate, renal, testicular
  • Other:
    • Vascular - haemangioma (Von Hippel-Lindau Syndrome)
    • Midline - dermoid/epidermoid cyst
    • Pineal: pinealblastoma/cytoma, germ cell Tx
86
Q

Astrocytomas

A

arise from astrocytes in any part of the brain

Diffusely infiltrative, with ill-defined capsule around tumour

WHO grading 1-4 (increasingly malignant)

  • Grd 1 (2%): pilocytic - median age 13yrs
  • Grd 2 (23%): diffuse - median age 40yrs
  • Grd 3 (30%): Anaplastic - median age 45yrs
  • Grd 4 (45%): glioblastoma Multiforme - median age >55yrs
87
Q

Oligodendroglioma

A

Arise from oligodendroglial cells

1p19q co-deletion is ‘genetic signanture’

Frontal lobe involvement is common

88
Q

Ependymoma

A

airse from ependymal cells e.g. 4th ventricle

2 peaks of incidence at age 5 and 35 yrs

89
Q

Lymphoma

A

Often intraventricular, increased risk with immunocompromise, may regress with steroids

90
Q

Meningioma

A

Arise from arachnoid cap cells

More common in females

Mostly parasagittal (attached to midline) & convex (over hemisphere surface)

Slow growing & usually benign

91
Q

Pituitary

A

Usually benign adenomas

May present with endocrine hyper/po function

Bitermporal hemianopia - upward compression of optic chiasm

92
Q

Cerebellopontine

A

acoustic neuroma often presents with sensorineural hearing loss & facial nerve palsy

Usually benign & surgery/radiosurgery is curative

93
Q

Metastases

A

small often multiple lesions with disporportionately excessive oedema

more common in pt aged >60yrs

Most = intra-axial

some = extra-axial (attached to dural surface)

Common primary lesions:

  • lung (60%) - small cell carcinoma
  • Breast (20%) - oestrogen receptor positivity predicts favourable response to chemotherapy
  • Others (20%): colon, melanoma, prostate, renal, testicular
94
Q

What are the clinical feautres of brain tumours?

A

depends on mechanism of involvement e.g. direct infiltration & destruction of neurones, local pressure on neighbouring structures or generalised increase in ICP

Clinical features incl:

  • Headaches (morning), nausea & vomiting, papilloedema (all due to raised ICP)
  • Drowsiness
  • Seizures
  • Focal neurological deficits:
    • hemiparesis (contralateral frontal involvement)
    • Dysphasia (broca/wernicke)
    • CN palsy, carioresp disturbance (brainstem involvement)
    • Ataxia, incoordination, hydrocephalus (cerebellum involvement)
95
Q

What are the radiological features of common brain tumours?

A

Dependent on the imaging modality & tumour

CT requires pre- and post- contrast scan comparison

MRI demonstrates if mets are solitary or multiple

Magnetic resonance spectroscopy can generate useful info re tumour activity

common imgaing findings:

  • Glioma (high grade): large lesion with central low density (necrosis), ring enhancement, rapid progression
  • Metastases: small & multiple, less ring enhancement c.f glioma, disproportionately excessive peri-tumour oedema
  • Meningioma: extra-axial, high density on non-contrast CT, slow progression
96
Q

What are the surgical treatment options & prognoses of gliomas?

A
  • Grd1: gross total surgical resection +/- radiotherapy
    • likely to be curative with total excision, especially in children
  • Grd2: surgical debulking depending on location. Chemotheray proven beneficial
    • 30% survival at 5 yrs, 85% transform into higher grade
  • Grd3: surgical debulking depending on location + adj radiotherapy. Chemotheray proven beneficial
    • median survival 2 yrs (with Rx)
  • Grd4:
  • surgical debulking depending on location + adj radiotherapy. Chemotheray proven beneficial
    • median survival 10mo (with Rx)
97
Q

What are the surgical treatment options & prognoses of metastases (brain)?

A
  • Non-small cell lung: surgical debulking/biopsy + radiotherapy
    • poor prognosis, depends on resection of primary and other extracranial mets
  • Breast: surgery, chemo, radiotherapy
    • can be >5yrs with full resection of a solitary brain met & chemosensitive Tx
98
Q

What are the surgical treatment options & prognoses of meningioma?

A
  • Curative surgery is usually feasible even with bone involvement. Radiotherapy indicated for all malignant meningioma
    • 90% cure
    • 5-10% recurrence if benign
    • 5% = malignant and have poor outcomes

RLH MRCS (22 decks)

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