Neuro Flashcards

1
Q

Name the three most common scoring systems in the UK for grading the severity of SAH

A

World Federation of Neurological Surgeons (WFNS) (clinical)
Hunt & Hess (clinical)
Fisher grade (CT grading)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the causes of SAH?

A

Rupture of berry aneurysm
Rupture of AVM
Traumatic SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name some risk factors for developing aneurysmal SAH

A
Smoking
Polycystic kidneys
Cocaine use
Amphetamine use
Ehler’s Danlos
Genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name some early neurological complications of SAH

A

Rebleeding
Seizure
Hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name some later neurological complications of aneurysm SAH

A

Delayed cerebral ischaemia/vasospasm
Cognitive impairment
Neurocognitive symptoms - low mood/sleep disturbance
Hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List some indications for awake craniotomy

A

Epilepsy surgery
Tumour resection in eloquent areas of brain
DBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List the absolute contraindications to awake craniotomy

A

Cannot lie still

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List the relative contraindications to awake craniotomy

A
Learning difficulties
Airway concerns - OSA
Chronic cough
Anxious patients
Language barrier
Children unable to cooperate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name 3 anaesthetic approaches to awake craniotomy

A
  1. Asleep -> awake
  2. Asleep -> awake -> asleep
  3. Sedation - awake throughout
  4. No sedation/regional only (uncommon)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What intraoperative adverse incidents may occur in an awake craniotomy?

A
Airway problems & hypoventilation
Conversion to GA required
Seizure
Air embolism
Patient intolerance/revoking consent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the flow of CSF in the brain

A

Choroid plexus in the LATERAL ventricles -> Foramen of Munro -> THIRD ventricle -> Sylvian aqueduct -> FOURTH ventricle -> Foramen of Magendie & Luschka -> spinal canal -> arachnoid villi ->dural venous sinuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the clinical features of acromegaly?

A
OSA
Coarsening facial features - macroglossia, prognathism, big ears
Carpal tunnel syndrome
Soft tissue changes - increased sweating, big hands
Headache
Hypertension
T2DM
Cardiomegaly/cardiomyopathy
Vocal cord hypertrophy - deep voice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

During trans-sphenoidal resection of pituitary tumour, the surgeon asks you to facilitate the descent of the pituitary into the operative field. How could you do this?

A
  • Controlled hypercapnoea (decrease MV)

- Injection of saline into a lumbar drain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What follow up do patients need post pituitary resection?

A

IGF-1 levels

Colonoscopy

Visual fields

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the endocrine complications of pituitary tumour resection?

A

Diabetes insipidus
Adrenocortical deficiency
Panhypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the neurosurgical complications post pituitary adenoma resection?

A

CSF leak/rhinorrhea

Vascular injury - carotid artery

Optic nerve injury

Nasal septum perforation

Infection - meningitis/sinusitis

Anosmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is secondary brain injury and when is it likely to occur?

A

Deleterious changes that happen over hours/days as a consequence of the initial injury
Mediated by inflammatory, neurogenic and vasogenic processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the pathophysiology of secondary brain injury?

A
  1. Reduced cerebral O2 delivery
  2. Increased CMRO2
  3. Cellular mechanisms

-Primary injury may exhaust compensatory capacity of brain (e.g. ICH) -> raising ICP & Monro Kelly Doctrine
-Inflammation/local tissue damage -> release of excitatory neurotransmitters causing calcium influx to cells and cell death
-Dying cells release free radicals causing increased blood vessel permeability and causing vasogenic fluid accumulation
-Loss of cerebral auto regulation
-Hypoxia/hypotension/hypercarbia/hypocarbia/hypoglycaemia/hyperglycaemia -> exacerbate secondary brain injury and inhibit auto-regulation
-Seizures cause raised ICP, raised CMRO2 and reduce PaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can secondary brain injury be minimised?

A
ABCDE:
Airway control -> I&V if low GCS/seizures/hypoxic/hypercarbia/unable to protect airway
C spine control
PaO2 >12
PaCO2 <4.5kPa
PEEP for oxygenation but otherwise avoid
Maintain MAP >80mmHg (or higher if ICP raised)
Allow good venous drainage - head neutral, head up etc
Catheterise
Seizure control
Temp control
BM control
Sedate to control CMRO2
ICP monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the grades of severity with the WFNS for SAH?

A
  1. GCS 15, no motor deficit
  2. GCS 13-14, no motor deficit
  3. GCS 13-14 with motor deficit
  4. GCS 7-12 with or without motor deficit
  5. GCS 2-6 with or without motor deficit
21
Q

What is autonomic dysreflexia?

A

Disorganised spinal sympathetic response to stimuli below the level of the lesion
Spinal circuits below the lesion are established and cause exaggerated responses

Sympathetic activation causes massive vasoconstriction and hypertension
Intact baroreceptors sense the hypertension causing reflex bradycardia
Descending inhibitory pathways not transmitted due to discontinuous cord

22
Q

What features of spinal cord injury are associated with development of severe autonomic dysreflexia?

A

Complete (rather than incomplete) spinal cord injury
Higher spinal cord lesions more severe
Usually >1 year after injury

23
Q

What are the mechanisms of cerebral autoregulation?

A

Metabolic - balance between demand and supply; vasoactive substances

Myogenic - transmural pressure

Neurogenic - vascular smooth muscle resistance via autonomic innervation

24
Q

Where can aneurysms form? Where is most common?

A
Anterior communicating (40%)
Middle cerebral/internal carotid
Posterior communicating
25
Q

What are the contents of the posterior fossa?

A
  • Brainstem (midbrain, pons, medulla)
  • Cerebellum
  • Fourth ventricle
  • Cranial nerves
26
Q

What are the PRE-OP considerations for anaesthetising a patient for posterior fossa surgery?

A
  • Documentation of deficits/evaluation of cranial nerves

- Assess for presence of raised ICP

27
Q

What are the INTRA-OP considerations when anaesthetising a patient for posterior fossa surgery?

A

Positioning - ETT/prone/pressure
Blood loss - sinuses
BP instability - brainstem, arterial line
Facial nerve monitoring - TIVA

How to give a Posterior Fossa anaesthetic:

  • Monitoring PLUS arterial line
  • Prepare for massive blood loss (and sudden too!)
  • TIVA with Remi
  • Facial nerve monitoring may be required (depending on tumour location etc e.g. acoustic neuroma)
  • Reinforced ETT
  • Positioning - prone/lateral/park bench
  • Mayfield clamp - stimulating
  • Cardiovascular instability when handling brainstem
  • Smooth extubation
28
Q

What are the POST-OP considerations for posterior fossa surgery?

A
  • HDU post op
  • Any new lower cranial nerve dysfunction will put them at risk for aspiration
  • Highly emetogenic - lots of anti-emetics prescribed
  • More painful than supratentorial surgery
29
Q

What is an acoustic neuroma?

A

A vestibular schwannoma

  • Benign tumour of myelin-forming Schwann cells of 8th cranial nerve
  • Clinical features - unilateral hearing loss, tinnitus, vertigo
  • If large: Trigeminal or Facial nerve features
30
Q

What are the normal CSF pressure waves and how do they relate to the cardiac cycle?

A

P1 > P2 > P3

A waves: pathological, high amplitude

B waves: rhythmic oscillations, mechanically ventilated patients

C waves: low amplitude, non pathological

(See “Monitoring the brain”)

31
Q

What is the normal range of ICP for adults and infants?

A

10-15mmHg

3-4mmHg

32
Q

Describe the types of ICP waves

A

A waves

B waves

C waves

33
Q

How do you measure ICP?

A

Invasively:
—ICP bolt
—EVD

Non-invasively:
—History of symptoms/change in symptoms
—Papilloedema
—CT/MRI
—USS of optic sheath diameter
34
Q

How can cerebral metabolism be monitored?

A

35
Q

What are the different spinal cord protection strategies undertaken during thoracoabdominal aneurysm repair?

A
  1. Mild systemic hypothermia (32 - 34)
  2. Maintaining Spinal Cord Perfusion Pressure (SCPP = MAP - CSFP) by pushing up MAP or lumbar drains for decreasing CSFP
  3. Distal aortic shunt through fem-fem/L heart bypass
  4. Pharmacological neuroprotection - free radical scavenging, steroids
  5. Monitoring spinal cord function with MEPs/SSEPs
36
Q

What are the afferent and efferent cranial nerves used for brain stem death testing?

A

Pupillary light reflex - II / III

Corneal reflex - V / VII

Supraorbital pain stimulus - V / VII, XI

Vestibulo-ocular - VII / III, IV, VI

Gag reflex - IX / X

Cough reflex - X / X

37
Q

What are the indications/preconditions for brainstem death testing?

A

Apnoeic coma

Clear diagnosis of underlying cause

38
Q

How is oxygenation maintained during apnoea testing?

A

Pre-oxygenate
Oxygen via catheter in ETT
Apnoeic mass transfer of O2 (by 250ml/min removal of O2 from FRC with only 10ml CO2 added = 240ml drawn down)

39
Q

What supportive tests are useful in brainstem death testing?

A
Cerebral angiography - MR/CT
Transcranial Doppler
EEG
PET
Evoked potentials
40
Q

How would you anaesthetise someone for scoliosis surgery?

A

Pre-op:
—Assessment of restrictive lung deficit & RV function - ECHO and spirometry
—Comorbidities - especially if associated condition (e.g. neuromuscular syndromes)

Intra-op:
—TIVA
—Spinal cord monitoring (reduces risk from 5% to 0.5% of damaging cord)
—Invasive monitoring - A-line/urinary catheter/IV access
—Positioning (prone)
—Reinforced ETT
—Blood loss preparation & TXA
—Attention to warming - high risk of heat loss

Post-op:
—HDU
—Good analgesia - paracetamol/NSAIDS/ketamine/Mg/IV lidocaine/opioid PCA/epidural catheter by surgical team
—Good PONV prevention

41
Q

Describe the analgesic regime for patients undergoing scoliosis surgery

A
Multimodal:
—IT opioids
—PCA
—NSAIDs
—Paracetamol
—Intraoperative remifentanil
—Intraoperative/postoperative ketamine infusion
—Magnesium

Control PONV
Keep warm

42
Q

How can you measure CSF pressure?

A

Directly:
—Lumbar Puncture
—Lumbar drain
—Intra-parenchymal sensor

Indirectly:
—Patient report
—Imaging

Normal CSF pressure is 10-15mmHg

43
Q

How can you measure cerebral oxygenation?

A

Jugular venous SpO2
NIRS
Brain tissue oxygenation

44
Q

How can you measure Cerebral Blood Flow?

A

Transcranial Doppler

CT/MRI perfusion scans

45
Q

What is the difference between Serotonin Syndrome and Neuroleptic Malignant Syndrome?

A

Serotonin Syndrome:
—Rapid onset; rapid improvement
—Hyperreactivity: tremor/clonus/hyperreflexia
—Treated with benzos

NMS:
—Slow onset
—Bradyreflexia, rigidity
—Caused by dopamine antagonist OR withdrawal of dopamine agonists
—Treated with bromocriptine; could use dantrolene
—Slow resolution
—Higher mortality than SS

46
Q

What is neurofibromatosis?

A

Autosomal dominant
Type 1:
—intellectual impairment, neural tumours, scoliosis, phaeochromocytoma, cardiomyopathy

Type 2:
—bilateral acoustic neuroma, cataracts, neural tumours

47
Q

What trial looked at decompressive craniectomy?

A

DESTINY trial looked at decompressive craniectomy in malignant MCA syndrome in patients >60years old

48
Q

What grading system is used in diffuse axonal injury?

A

Marshall grading system (1-4)
Midline shift of >5mm = Grade 4

49
Q

What factors affect cerebral blood flow?

A

Those affecting:
—Cerebral Perfusion Pressure:
-MAP
-ICP
-CVP
—Radius of cerebral vessels:
-Myogenic control
-Metabolic mediators: pCO2, pO2, CMRO2, Temp
-Neurogenic mediators
-Endothelial mediators
-Chemical mediators: volatile or IV anaesthetic agents
—Affecting blood rheology:
-Haematocrit