3 - Neurological Emergencies Flashcards

1
Q

What is a bulbar palsy and how does it present?

A

LMN lesion of CN 9, 10 and 12 causing issues with speech and swallowing

- Flaccid fasiculating tongue

- Absent or normal jaw jerk reflex

- Absent gag reflex

- Nasal quiet speech

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2
Q

What are the cause of an acute bulbar palsy

(Image important)

A
  • GBS
  • Myasthenia Gravis
  • Stroke (Lateral Medullary Syndrome)
  • MND
  • Syringobulbia
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3
Q

What is a pseudobulbar palsy?

A

A bilateral lesion of the corticobulbar tracts so affects CN 9, 10 and 12

UMN lesion of speech and swallow

Has to be bilateral lesion as CN nuclei have bilateral input

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4
Q

How does pseudobulbar palsy present?

A

Presentation

  • Spastic tongue
  • Increased jaw jerk reflex
  • Slow deliberate speech
  • Increased gag reflex
  • Emotional lability
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5
Q

What are some causes of pseudobulbar palsy?

A

- Vascular: bilateral internal capsule stroke

- Degenerative: MND, progressive supranuclear palsy

- Autoimmune: MS

- Upper brain stem tumours

- Trauma

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6
Q

How is the pseudobulbar affect treated?

A

Dextromethorphan and Quinidine

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7
Q

Why is temporal arteritis an emergency?

A

Bilaterally sight threatening vasculitis!!!!!

Also a stroke risk

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8
Q

What symptoms should make you consider temporal arteritis?

A
  • Headache
  • Scalp tenderness
  • Jaw claudication
  • Sudden unilateral blindness
  • Amaurosis Fugax
  • History of PMR
  • >55
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9
Q

What investigations should you do if you suspect GCA?

A
  • CRP and ESR: raised

- FBC: normocytic anaemia, raised platelets

- LFTs: raised ALP

- Temporal artery biopsy: within 14 days of starting steroids, take around 3-5cm due to skip lesions, if nothing then biopsy asymptomatic side too

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10
Q

What is the management for a suspected case of GCA?

A

- Immediate high dose steroids: before TAB (60mg PO prednisolone) to prevent blindness and stroke

- Low dose aspirin

- PPI: Gastric protection

- Bisphosphonate and Adcal: Bone protection

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11
Q

What is the prognosis with GCA?

A

Usually a 2 year course then full remission if tapered slowly

Wean down prednisolone as symptoms improve and ESR declines

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12
Q

What are some signs of respiratory distress?

A
  • Tachypnoea
  • Nasal Flaring
  • Tracheal tug
  • Use of accessory muscles
  • Intercostal, subcostal and sternal recession
  • Pulsus paradoxus
  • Abnormal sounds
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13
Q

How do you manage a respiratory arrest?

A

- Call for help

- Check pulse every 2 minutes

- Head-tilt-Chin-lift (if C-Spine injury do jaw thrust)

- Bag Valve Mask every 5-6 seconds

  • Consider oral or nasopharyngeal adjunct
  • Prepare for advanced airway e.g laryngeal mask

- 15L supplemental oxygen through BVM

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14
Q

What are some neurological causes of respiratory distress/arrest?

A

- Drive Failure: centrally acting drugs, tonsillar herniation due to raised ICP, Stroke

- Transmission Failure: GBS, MG, Spinal Cord Lesion, MND

- Action Failure: Muscular dystrophies, myopathies

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15
Q

How can you manage respiratory distress?

A

Ix:

  • CXR
  • ABG
  • Review drug chart e.g opioids
  • U+Es

Mx:

  • Oxygen
  • CPAP
  • Consider need for invasive ventilation
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16
Q

Head trauma patients are treated with an ABCDE approach. What are some alterations made in the A to E process when there is head trauma?

A
  • Do not use nasopharyngeal airway as can cause damage if skull fracture
  • Do not do Head-tilt-Chin-lift if C-Spine injury, do Jaw Thrust
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17
Q

What is the immediate management for a patient with a head injury?

A

- Stabilise C-spine, Airway, Breathing and Circulation

- Assess GCS: If 8 or less need urgent ICU involvement to manage airway

- Assess antegrade/retrograde amnesia

- Neurological examination: start neuro obs

- Consider need for imaging

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18
Q

Whay is the criteria for performing a CT head scan within 1 hour of head injury? (immediately)

A
  • GCS <13 on initial assessment
  • GCS <15 at 2 hours after the injury on assessment in ED
  • Suspected open or depressed skull fracture
  • Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, CSF from the ear or nose, Battle’s sign)
  • Post-traumatic seizure
  • Focal neurological deficit.
  • More than 1 episode of vomiting.
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19
Q

What parameters are included in neuro obs and how often should they be taken?

A
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20
Q

What is the criteria for performing a CT head scan within 8 hours following head injury?

A

Any loss of consciousness or amnesia since the injury AND ONE OF:

- Aged 65 or more

- History of bleeding or clotting disorders (inc taking warfarin)

- High-impact injury (e.g fall>1m or >5 stairs or struck by moving vehicle)

- Retrograde amnesia >30 minutes

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21
Q

For suspected cervical spine injuries, when should you perfor a CT cervical spine within an hour?

A
  • GCS <13 on initial assessment
  • Patient has been intubated
  • Definitive diagnosis of cevical spine injury is needed urgently e.g beforre surgery
  • Patient is having other body areas scanned e.g multitrauma
  • See image
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22
Q

When should you discuss a patient with a headinjury with the neurosurgeons?

A
  • Significant abnormalities on CT
  • Persistent GCS of 8 or less
  • Deteriorating GCS
  • Focal neurology
  • Seizure without full recovery
  • CSF LEAK
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23
Q

What are some complications of a head injury?

A

Early

  • Extradural/subdural haemorraghe
  • Seizures

Late

  • Subdural
  • Seizures
  • Diabetes Insipidus
  • Parkinsonism
  • Dementia
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24
Q

What are some causes of impaired conscious level/coma?

A

Metabolic: drugs, alcohol, CO, hypoglycaemia, hypothermia, sepsis, hypoxia

Neurological: trauma, meningitis, tumour, stroke, haemorraghe, epilepsy

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25
Q

How do you manage a patient that has arrived in ED comatosed?

A

A to E:

  • Consider intubation if GCS<8
  • Give O2 and treat any seizures
  • Protect cervical spine
  • Checl BM
  • IV naloxone if opioid intoxication, IV flumazenil if benzodiazepine intoxication and airway compromise

Full Body Exam

Collalteral History:

  • How they were found
  • Recent complaints and PMHx inc DHx
  • Drug or Alcohol Exposure

Arrange Urgent CT head

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26
Q

How do you calculate GCS?

A

Best response

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27
Q

How may spinal cord compression present?

A

- Bilateral leg weakness (arms if C-spine)

- Sensory level

- Preceding back pain

- Bladder and anal sphincter (involved late, hesitancy/frequency/retention)

- LMN sign at level of lesion, UMN below: remember acute cord compression may show LMN signs e.g reduced reflexes but actually be UMN

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28
Q

What are some causes of spinal cord compression?

A

- Trauma

- Metastases from BLTKP

- Infection (especially TB in at-risk patients)

- Disc prolapse

- Epidural haematoma (on warfarin)

- Myeloma

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29
Q

How is suspected spinal cord compression investigated and managed? (same as CES)

A

Ix

- Urgent whole spine MRI

- PR Exam

  • CXR: metastases, TB
  • Bloods: FBC, ESR, B12, U+Es, LFTs, PSA, serum electrophoresis

Mx

  • Urgent dexamethasone if malignancy given daily with PPI cover
  • Surgical decompression (laminectomy) within 48 hours as otherwise permanent neurological deficits
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30
Q

What are some differential diagnoses for spinal cord compression?

A
  • Transverse myelitis
  • MS
  • GBS
  • Spinal artery thrombosis or aneurysm
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31
Q

What is the difference in presentation between spinal cord compression and cauda equina syndrome?

A
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32
Q

How can metastases cause spinal cord compression?

A
  • Collapse of vertebrae
  • Extension of tumour into cord
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33
Q

What is the difference in presentaion between cauda equina and conus medullaris syndrome?

A

CES

  • Back and radicular leg pain
  • Asymmetrical atrophic areflexic paralysis of legs (LMN)
  • Sensory loss in root distribution
  • Decreased sphincter tone

Conus Medullaris

  • Mixed UMN/LMN
  • Leg weakness
  • Early urinary retention and constipation
  • Back pain
  • Sacral sensory disturbance
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34
Q

What is the definition of a stroke?

A

Cerebrovascular event that is caused by abnormal perfusion of cerebral tissue

Sudden onset of rapidly developing focal or global neurological disturbance, which lasts more than 24 hours

Ischaemic or Haemorraghic

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35
Q

How are strokes classified?

A
  • Ischaemic (85%): Oxford/Bamford Classification
    • Haemorraghic (15%): Intracerebral or SAH
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36
Q

What are some causes of stroke?

A
  • Ischaemic: Thrombosis, Emboli, Dissection
  • Haemorraghic: HTN, AV malformation, Trauma, Bleeding disorders, Vasculitis
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37
Q

What are some risk factors for a stroke?

A
  • Smoking
  • Diabetes mellitus
  • Hypertension
  • Hypercholesterolaemia
  • Obesity
  • Atrial fibrillation
  • Carotid artery disease
  • Age
  • Thrombophilic disorders (e.g. antiphospholipid syndrome)
  • Sickle cell disease
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38
Q

What is the blood supply to each part of the brain?

A

Anterior Circulation: From ICA

Posterior Circulation: From Vertebrobasilar circulation

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39
Q

What are the different classifications of stroke in the Bamford/Oxford classification?

A

Remember criteria at bottom of table

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40
Q

What are some of the signs and symptoms of the following types of strokes:

  • Haemorraghic
  • Anterior Ischaemic
  • Posterior Ischaemic
A

Haemorraghic

  • Headache
  • Altered mental status
  • Nausea & Vomiting
  • Hypertension
  • Seizures
  • Focal neurological deficits

Anterior Ischaemic

  • Unilateral contralateral weakness and/or sensory deficit: face and/or arms and/or legs
  • Homonymous hemianopia
  • Higher cerebral dysfunction: dysphasia, visuospatial dysfunction (e.g. neglect, agnosia)

Posterior Ischaemic

  • Dizziness
  • Diplopia
  • Dysarthria & Dysphagia
    • Ataxia
  • Visual Field defects
  • Brainstem syndromes (ipsilateral cranial nerve lesions with contralateral sensory and motor limb deficits)
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41
Q

What is Wallenburg and Locked-In Syndrome?

A

Wallenburg/Lateral Medullary syndrome

  • Posterior inferior cerebellar artery occlusion
  • Nystagmus, Vertigo, Ipsilateral Horner’s syndrome, Ipsilateral facial sensory loss, Dysarthria & dysphagia
  • Diplopia
  • Contralateral pain and temperature loss
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42
Q

What are two scoring systems used for an acute stroke?

A

FAST

  • Used in the community to decide whether a patient needs transfer to a hyper acute stroke unit
  • Any new arm weakness, facial weakness, new speech difficulty

NIHSS

  • In hospital to decide whether to do thrombolysis and the clinical outcome
  • Score <4 is good clinical outcome
  • Score >22 is high and risk of haemorraghe with thrombolysis as larger proportion of ischaemia
  • Score of 26 or more is contraindication for thrombolysis
43
Q

What are some examples of ‘stroke mimics’?

A
44
Q

What investigations are done when an acute stroke is suspected?

A

CT HEAD TO SEE IF ISCHAEMIC OR HAEMORRAGHIC

  • Bedside: observations, blood glucose, ECG (AF)
  • Bloods: FBC, U&Es, Bone profile, LFT, ESR, coagulation, lipid profile, HbA1c
  • Imaging: CT head +/- CT angiography +/- MRI head
    • Special: Echo, carotid dopplers, 24 hour tape, young stroke screen
45
Q

What is the acute management for a stroke?

A
  1. Protect airway
  2. Maintain homeostasis: Blood glucose (4-11) and BP
  3. Screen swallow: NBM until screen
  4. CT/MRI within 1hr
  5. Aspirin 300mg if haemorraghic stroke ruled out
  6. Thrombolysis (Alteplase) if haemorraghic stroke ruled out and <4.5 hours since onset. Also consider thrombectomy
  7. If haemorraghic stroke consider need for decompressive hemicraniectomy
46
Q

What is the secondary management for a stroke after initial management has taken place?

A

Secondary Prevention:

  • Clopidogrel 75mg once daily
  • Atorvastatin 80mg should be started but not immediately
  • Carotid endarterectomy or stenting in patients with carotid artery disease
  • Treat modifiable risk factors such as hypertension and diabetes
47
Q

What are some complications with a stroke?

A
48
Q

What is a malignant MCA infarction?

A
  • Rapid neurological deterioration due to cerebral oedema following an MCA infarct
  • Need urgent decompressive hemicraniectomy
49
Q

What advice should you give somebody on driving following a stroke?

A
  1. Cars and motorcycles: stop driving one month. Inform DVLA if ongoing symptoms after one month
  2. Larger vehicles (e.g. buses, lorries): stop driving, inform the DVLA
50
Q

What is the gold standard imaging following a stroke?

A

Diffusion-Weighted MRI

Often do CT as faster and can exclude haemorraghic. Can also do Carotid Doppler US to see if need to do endartectomy

51
Q

What is a TIA and how may it present?

A

Ischaemic neurological event with symptoms lasting <24h, patient’s often go on to have a full stroke within a week of a TIA

  • Amaurosis Fugax
  • Unilateral weakness or paraesthesia
  • Rare to have global events e.g dizzy, syncope
  • Crescendo TIA: more than 2 in a week suggests critical stenosis in superior division MCA
52
Q

What investigations are done when a patient has a TIA?

A
  • FBC
  • U+Es
  • Glucose
  • Lipids
  • CXR
  • ECG
  • Carotid Doppler and Angiograph
  • CT or Diffusion Weighted MRI
  • Echo
53
Q

How is a TIA treated?

A
  • Control risk factors: Optimise BP, DM, stop smoking
  • Aspirin 300mg: for 2 weeks then switch to Clopidogrel 75mg
  • Anticoagulate if AF
  • Carotid Endarctectomy within 2 weeks if critical stenosis
  • Do not drive for a month
  • Calculate ABCD2 score
54
Q

What is the ABCD2 score?

A

Stratifies which patients are at higher risk of having a stroke following a TIA

Score of 4 or more patient is at high risk of early stroke so see within 24h

Score of 6 or more predicts stroke in next 2 days

55
Q

What is status epilepticus?

A
  • Seizure lasting > 5 minutes
  • Repeated seizures without regaining full consciousness/recovery between episodes
  • High risk of permanent brain damage so assume status when seizure at 5 minute mark
56
Q

What are the different stages of status epileptics and what happens in each stage?

(important image)

A

1st Stage - Early Status (0-10 minutes)

  • Check for safety and call for help
  • ABCDE
  • Protect airway and provide oxygen therapy 100%
  • Protect patient, but do not restrain
  • Establish IV access and take bloods

2nd Stage (0-30 minutes)

  • Regular monitoring (e.g. cycling observations, ECG monitoring if possible, temperature)
  • Emergency AED therapy
  • Emergency investigations (bloods, CXR, toxicology screen)
  • Consider alcohol intoxication: consider Parbinex
  • Blood glucose level: consider intravenous glucose (e.g. 100 mls 20%)

3rd Stage - Established Status (0-60 minutes)

  • Determine aetiology (collateral history, hospital records)
  • Further emergency AEDs
  • Alert anaesthetic team and ITU
  • Treat any co-morbidities (i.e. sepsis)
  • Consider urgent CT head (e.g. exclude intracerebral bleed, structural abnormalities)

4th Stage - Refractory Status (30-90 minutes)

  • Transfer to ITU: requires general anaesthesia with intubation and ventilation
  • EEG monitoring
57
Q

What is some basic seizure first aid?

A
58
Q

What are the emergency drugs used for status epilepticus?

A
  • Benzodiazepine (IV Lorazepam 4mg/0.1mg per Kg, Diazepam 10mg PR, Midazolam 10mg Buccal): At 5 minutes
  • Benzodiazepine: Another dose 10-20 minutes later
  • IV Phenytoin Loading: 15-18mg/kg IVI at a rate of 100mg/minute, needs ECG monitoring as risk of hypotension, bradycardia and heart block.

Can also use phenobarbital

  • Seek ICU Help: put under general anaesthesia for 12-24 hours guided by EEG monitoring, use Propofol, Midazolam, Thiopental sodium
59
Q

If a patient is in status epilepticus and you suspect the patient has alcoholism or malnourishment, what other pharmacological treatment should you give them?

A
  • Thiamine 250mg IV over 30 minutes before glucose as risk of making Wernicke’s worse
  • Glucose 50ml 50% IV
60
Q

What investigations are important in status epilepticus?

A
  • O2 sats and BMs (reversible seizure causes)
  • ABG
  • Bloods: FBC, U&E, LFT, CRP, Ca, Mg, clotting. Take when gaining IV access
  • Serum and Urine: toxicology, AED levels
61
Q

What are some of the acute and chronic complications of Status Epilepticus?

A
  • Acute: hyperthermia, cardiac arrhythmias, severe hypoxaemia, shock, cerebral oedema, death
  • Chronic: long-term neurological damage (epilepsy, focal neurological deficits, encephalopathy)
62
Q

What organisms are most common in meningitis?

A
  • Meningococcus
  • Pneumococcus
  • H.Influenzae
  • Listeria Monocytogenes
  • HSV
  • VSV
  • CMV
  • TB
  • Cryptococcus neoformans
63
Q

What are the features of meningitis?

A

Early

Headache, fever, cold hands and feet, abnormal skin colour

Late

  • Meningism: neck stiffness, photophobia, Kernig’s signs
  • Reduced GCS
  • Seizures
  • Petechial rash
  • Shock
64
Q

What is the management of suspected meningitis?

A

Do Ix and Mx in parallel

  • Signs of raised ICP contact ICU immediately
  • Isolate for 24h and inform public health
  • SEPSIS 6 if necessary
  • Blood Cultures and LP: if no signs of raised ICP, shock or petechial rash
  • IV abx: Ceftriaxone. Add Amoxicillin if >60 years old to cover Listeria, IV acyclovir if Viral
  • IV dexamethasone: 10mg/6h if signs of meningism
  • Ix: U+E, FBC, LFT, Glucose, Coagulation, Bacterial and Viral Throat swab
  • Prophylaxis
65
Q

If a patient is suspected to have meningitis in primary care, what should the GP do?

A

Give benzylpenicillin 1.2g IM before admitting

66
Q

When should you do a CT head in the work up for meningitis?

A

Urgent CT Head scan before LP if signs suggestive of a shift of brain compartments

  • GCS ≤12
  • Focal neurological signs
  • Papilloedema
  • Continuous or uncontrolled seizures
67
Q

What is the second line empirical antibiotic for meningitis?

A

Viral meningitis is supportive with rest, hydration, analgesia and antipyretic

68
Q

What will a LP show in bacterial, viral and TB meningitis?

(IMPORTANT IMAGE)

A
  • Opening pressure
  • Cell count and differential
  • Protein
  • Glucose (paired with serum glucose)
  • Microscopy, cultures & sensitivity (MC&S)
  • Viral PCR
  • Save sample (can subsequently be used to run other tests)
  • Others (if indicated): cryptococcal antigen (paired with serum), TB PCR
69
Q

After notifying PHE about a case of meningitis, what other public health measures do you need to take?

A
  • Isolate patient in side room for 24h
  • Contact trace (household and kissed on mouth)
  • Give contacts Ciprofloxacin 500mg PO or Rifampicin regardless of vaccination status
  • Check MenB and MenACWY status
70
Q

What are some complications with meningitis?

A
71
Q

What is encephalitis and how may it present?

A

Inflammation of the brain parenchyma, suspect in anyone with odd behaviour

  • Altered mental status or confusion
  • Fever
  • Flu-like prodrome
  • Early seizures
72
Q

Should you CT after a head injury and if so, when?

A
73
Q

What are some causes of encephalitis?

(most common cause is underlined)

A
  • Viral: HSV-1 or 2 (fatal if not treated), CMV, EBV, VSV, HIV
  • Non-Viral Infectious: Mycoplasma, Tuberculosis, Rickettsial infections, Histoplasmosis and parasites (e.g. Echinococcus)
  • Paraneoplastic
  • Autoimmune
74
Q

What is post infectious encephalitis?

A
  • Acute disseminated encephalomyelitis (ADEM)
  • Demyelinating condition affecting CNS
  • Development of encephalopathy (e.g. confusion, altered mental status, irritability) and other neurological signs (e.g. hemiparesis, cranial nerve palsy, myelopathy)
  • 4-13 days following an infection or vaccination.
75
Q

What is autoimmune encephalitis?

A
  • Antibody against antigen in the CNS. Cause inflammation of the CNS
  • NMDA Encephalitis: psychiatric manifestations (e.g. agitation, bizarre behaviour, hallucinations, delusions), memory deficits, sleep deficits, seizures, altered mental status and autonomic instability (e.g. hyperthermia, fluctuations in blood pressure).
76
Q

What are the different types of autoimmune encephalitis?

A
77
Q

How can you tell the difference between encephalitis and meningitis?

A

Altered mental status in encephalitis!!!

78
Q

What investigations should you do if you suspect encephalitis?

A
  • Bedside: observations, urinalysis, ECG, sputum cultures
  • Bloods: full blood count, urea & electrolytes, bone profile, liver function tests, CRP, blood cultures, coagulation
  • Imaging: chest x-ray, CT head
  • Neuroimaging: MRI, CT
  • EEG
  • LP for CSF
  • Serology: autoantibodies
79
Q

Where do you often see HSV damage on neuroimaging?

A
  • Temporal lobes
  • Bilateral multifocal haemorrhage
80
Q

How is encephalitis managed?

A
  • IV acyclovir within 30 minutes (10mg/kg/8h) for 14 days
  • 2g IV Ceftriaxone BD to cover for meningitis
  • HDU or ICU transfer
  • Symptomatic treatment e.g Phenytoin for seizures

70% mortality if left untreated

81
Q

When should you suspect a cerebral abscess?

A

Suspect in any patient with raised ICP especially if fever and raised WCC

  • Seizures
  • Fever
  • Localising signs
  • Signs of raised ICP
82
Q

What investigations and management should you do for a cerebral abscess?

A

Ix:

  • CT/MRI (Ring-Enhancing Lesion)
  • FBC and ESR (raised WCC and ESR)
  • Biopsy

Mx:

  • Urgent neurosurgical referral
83
Q

What are the signs and symptoms of a SAH (bleed between arachnoid and pia mater)?

A

Symptoms

  • Thunderclap sudden onset headache
  • Sentinel headache
  • Vomiting
  • Seizures
  • Coma

Signs

  • Neck stiffness/Meningism
  • Kernig’s sign (after 6h)
  • Focal neurology e.g pupil changes
84
Q

SAH are often caused by AV malformations or a burst of a berry aneurysm.

What are some risk factors for a SAH?

A
  • Hypertension
  • Smoking
  • Excessive alcohol consumption
  • Cocaine use
  • Family history
  • EDS
  • Polycystic Kidney disease
  • Marfan’s
  • Sickle Cell Disease
85
Q

What investigations do you do if you suspect a SAH?

A
  • Urgent Non-Contrast CT head: hyperattenuation
  • LP: if -ve CT, do >12h after headache onset to look for xanthochromia (bilirubin from breakdown of RBCs, differentiates from traumatic tap)
  • Cerebral angiography: gold standard for detection, demonstration and localisation of ruptured aneurysms
86
Q

How is a SAH managed?

A

IMMEDIATE REFFERAL TO NEUROSURGERY

Supportive: Analgesia, Antiemetic, Fluid resus (Keep SBP<160)

Medical:

Nimodipine to reduce cerebral vasospasm and consequent cerebral ischaemia.

Can also give Levetiracetam if seizures or risk of

Surgical: Coiling or Clipping of aneurysm

Monitoring: for complications

87
Q

What are the complications with a SAH?

A
  • Rebleeding: common in first few days
  • Cerebral Ischaemia: due to vasospasm, can cause permanent neurological deficit
  • Hydrocephalus: due to blockage of arachnoid granulations, needs ventricular or lumbar drain
  • Hyponatraemia: do not fluid restrict
88
Q

How may a posterior communicating artery aneurysm present?

A

CNIII palsy

89
Q

How may a posterior communicating artery aneurysm present?

A

CNIII palsy

90
Q

What is a subdural haemorrhage and how does it appear on CT?

A

Collection of venous blood between dura and arachnoid due to damage to bridging veins

Presentation: Headache, nausea or vomiting, confusion, and diminished GCS

CT: Crescent shape not limited by sutures. Check if bilateral

Risks: Elderly due to atrophy, Trauma, Alcohol, Anticoagulants

91
Q

How is a subdural haematoma managed?

A
  • Urgent reversal of any clotting abnormalities
  • >10MM OR with midline shift>5mm then need craniotomy or burr hole
92
Q

What is the pathophysiology of an extradural haemorrhage and how does it appear on CT?

A

Rupture of the middle meningeal artery after a blow to temporoparietal region. Blood between skull and dura

CT: Biconvex limited to sutures

LP is contraindicated

93
Q

How may an extradural haemorrhage present?

A
  • Traumatic head injury
  • Transient LOC
  • Lucid interval for few hours then rapid decline in GCS
  • Headache
  • Vomiting
  • Ipsilateral pupil dilates
  • Can lead to death if left as respiratory arrest from brainstem compression
94
Q

How is an extradural haemorrhage managed?

A
  • Urgent transfer to neurosurgical unit
  • Clot evacuation and ligation of bleeding vessel
  • Consider need for intubation
95
Q

What are the principles of management for any intracranial bleed?

A
96
Q

What is classed as a raised ICP and what are some causes of this?

A
  • <15mmHg is normal
  • 20-25mmHg needs treatment
  • >40mmHg is severe life threatening

Could be mass effect, oedema or obstruction to fluid outflow

97
Q

f

A

f

98
Q

What are some of the features of a raised ICP?

A

Early

  • Morning headache: worse on coughing, leaning forward
  • Vomiting
  • Altered GCS

Late

  • Cushing’s Triad
  • Opthalmoplegia
  • Coma
  • Death
  • Seizures
99
Q

What signs on examination may you see with raised ICP?

A
  • Papilloedema with loss of venous pulsation
  • Occular palsies
  • Pupillary constriction then dilation
100
Q

What investigations should you do if you suspect a raised ICP?

A
101
Q

How is a raised ICP managed?

(image important!!!)

A

Need to lower ICP and avert secondary injury

  • Urgent Craniotomy or Burr Holes if focal causes
  • ICP monitor or bolt to monitor pressure
102
Q

What are the different types of herniation that can occur with raised ICP and how do they present?

A

Uncal: Lateral Supratentorial mass. Temporal lobe herniates to midbrain, CNIII compressed so ipsilateral dilated pupil and diplopia. Can lead to coma as compressing reticular activating system

Cerebellar Tonsil: Posterior fossa mass. Cerebellar tonsils through F.Magnum causing ataxia, upping plantar reflexes, LOC, Cushing’s triad, irregular breathing

Subfalcine (Cingulate): Frontal mass. Medial Frontal Lobe forced under rigid Falx Cerebri. Can compress ACA so stroke (contralateral leg weakness)

103
Q

What are some red flags for raised ICP?

A
103
Q

What are some red flags for raised ICP?

A