Neurosurgery

Question 1

Name and describe the red flags of back pain that require urgent investigation.

Answer 1

• <20 (infection, spondyloarthropathy, tumour)
• > 50 (crush fracture, multiple myeloma)
• persistant pain (tumour, infection)
• worse at morning/night (inflammatory, infectious, malignant causes)
• systemic illness, fever, weight loss (tumour, infection)
• thoracic pain (+ gait disturbance = cervical myelopathy)

Question 2

Describe the risk factors, presentation, and management of mechanical back pain.

Answer 2

• Risk factors: obesity, lack of exercise, female, chronic pain syndromes (e.g., fibromyalgia), psychosocial (e.g. dissatisfaction with work)
• Presentation: 20-60, several previous ‘flare ups’, no red flag symptoms
• Management: physiotherapy and NSAID analgesia 1st line

Question 3

Describe the pathology of spinal stenosis.

Answer 3

• central spinal canal is narrowed by one of three main causes: tumour, disc prolapse, or degenerative changes.
• degenerative changes are the most common. these include progressive loss of disc height, OA of facet joints, osteophytes, and buckling of the ligamentum flavum.

Question 4

Describe the differences between vascular and neurogenic claudication.

Answer 4

• Both may present with cramping, tingling, numbness, and pain.
• in neurogenic claudication, pain is relieved by leaning forwards (less pain on walking uphill, positive ‘shopping trolley’ sign)
• in neurogenic claudication, recovery is slower, pulses are present, and sensory symptoms are greater than in vascular claudication

Question 5

Describe the investigation and management of spinal stenosis.

Answer 5

• exclude cauda equina syndrome (bilateral sciatica, saddle anaesthesia, urinary symptoms, faecal symptoms, reduced anal tone, impotence)
• MRI to demonstrate canal narrowing
• Mx is with laminectomy

Question 6

Describe cauda equina syndrome (CES).

Answer 6

• compression of all nerve roots of the cauda equina, affecting sacral nerves (which control defaecation and urination)
• symptoms can include
• • bilateral leg pain
• • parasthesia and numbness, including saddle anaesthesia (perineum)
• • urinary incontinence, retention, faecal incontinence, constipation
• • reduced anal tone, demonstrated by PR exam
• urgent MRI with contrast is required
• management is urgent surgical decompression

Question 7

Describe the pathology of cervical myelopathy.

Answer 7

• compression of the spinal cord within the cervical region
• causes include spondylosis, stenosis, cervical disc herniation, malignancy, and ossification of the posterior longitudinal ligament (OPLL)
• risk factors: smoking, genetics, and occupation (those exposing patients to high axial loading)

Question 8

Describe the presentation of cervical myelopathy.

Answer 8

Cervical myelopathy causes UMN symptoms.
* ‘Do your fingers feel fat like a bunch of bananas?’
* Can you thread a needle? (fine finger movement)
* Do your legs jump at night? (duvet irritation elicits hyperreflexia)
* Do you feel like you’ll fall over in the shower with your eyes closed? (reduced proprioception)

Question 9

Describe the examination findings and differential diagnosis of cervical myelopathy.

Answer 9

• ankle clonus
• hyperreflexia in both extremities
• positive Babinski reflex
• Hoffmann’s sign (in 80%): gentle flicking of the nail results in twitching of other fingers
• DDx: MND (ALS), syringomyelia, spinal malignancy, MS

Question 10

Describe the investigation and management of cervical myelopathy.

Answer 10

• MRI is gold standard, but CT myelogram may be used if unavailable/contraindicated
• Urgent referral to specialist spine services (neurosurgery, orthopaedic spinal surgery)
• the condition does not improve without surgery. early surgery may offer chance at recovery, but for most patients, surgery prevents worsening but does not treat symptoms
• an anterior approach is best for 1-2 vertebral level involvement, whereas a posterior approach is best for 3+

Question 11

Describe the pathology and general presentation of sciatica.

Answer 11

• the nucleus pulposis of an intervertebral disc herniates through a disc tear
• herniation of the disc onto nerve roots causes symptoms; in the sciatic nerve distribution, this is sciatica
• symptoms include neuralgic pain, lower back pain, paraesthesia, numbness, and neurological signs
• sciatica is typically unilateral, as the posterior longitudinal ligament is thickened in the centre, meaning disc herniation goes to points of weakness at the side
• the straight leg raise is positive in lower lumbar disc prolapse (L5-S1), whereas the femoral stretch test is positive in upper lumbar disc prolapse (L3-4).

Question 12

Describe the changes seen in an L3 radiculopathy.

Answer 12

• sensory loss: anterior thigh
• motor weakness: knee extension (quadriceps)
• reflexes: decreased patellar
• stretch: positive femoral stretch test

Question 13

Describe the changes seen in an L4 radiculopathy.

Answer 13

• sensory: anterior thigh, inner leg
• motor: knee extension (quadriceps)
• reflexes: decreased patellar
• test: positive femoral stretch test

Question 14

Describe the changes seen in an L5 radiculopathy.

Answer 14

• sensory: lateral thigh and leg, extending to the dorsum of the foot
• motor: reduction in foot inversion and dorsiflexion
• reflexes: no change
• test: straight leg raise positive (tests the sciatic nerve)

Question 15

Describe the changes seen in S1 radiculopathy.

Answer 15

• sensory: posterolateral thigh and leg, extending to the plantar surface of the foot and little toe
• motor: reduction in plantarflexion
• reflexes: reduced ankle
• test: straight leg raise positive (tests sciatic nerve)

Question 16

Describe the management of sciatica.

Answer 16

• initial management is conservative, including 6 weeks of NSAIDs +/- PPIs and physiotherapy.
• presence of foot drop (L4) is a poor indicator and may require expedited surgical management
• image-guided epidural or nerve root canal (MRI first line) reduces pain rapidly
• in cases refractory to conservative management, discectomy may be indicated. in cases where osteophytes play a role, surgical decompression and trimming may play a role.

Question 17

Describe the pathology, risk factors, presentation, investigation, and management of subarachnoid haemorrhage (SAH).

Answer 17

• pathology: most SAHs occur secondary to a ruptured saccular (‘berry’) aneurysm, most often found at major arterial branch points in the circle of Willis
• risk factors: hypertension, smoking, disorders of collagen (EDS, ADPKD, coarctation of the aorta)
• presentation: thunderclap headache (‘the worst headache of my life’)
• investigation pivots around timing. a CT non-contrast is performed
  — if CT is negative and performed <6hr of headache onset, consider an alternative diagnosis
  — if CT is negative and performed >6hr of headache onset, wait until >12hr and perform a lumbar puncture (LP), which may show RBCs in the CSF (xanthochromia)
• management:
  — reverse anticoagulation
  — give nimodipine, a CCB, to prevent vasospasm
  — surgical coiling is first line, however craniotomy and clipping is an alternative
  — SIADH is a notable complication of surgery

Question 18

Describe the anatomy, clinical features, imaging features, and management of extradural (‘epidural’) haematoma.

Answer 18

• anatomy: haematoma between the dura mater and skull, commonly due to breakage of the pterion and middle meningeal artery
• clinical features: occurs due to ‘low-impact’ trauma (e.g. blow to the head, fall) with a lucid interval and fixed, dilated pupil
• imaging: CT first line. as the haematoma is limited by suture lines, CT will show a biconvex collection
• management depends on whether there is a neurological deficit.
  – no deficit: clinical and radiological observation
  – definitive: craniotomy and evacuation of the haematoma

Question 19

Describe the anatomy, clinical features, imaging features, and management of subdural haematoma.

Answer 19

• anatomy: between the dura and arachnoid mater. occurs due to laceration to the bridging veins. haematoma is not limited by suture lines.
• clinical features: seen mainly in the elderly and alcoholics. fluctuating consciousness.
• imaging: CT first line. shows a crescent-shaped concavity which may be hyperdense (acute) or hypodense (chronic)
• management: conservative (chronic or incidental finding), surgical decompression with burr holes (confused, neurological deficit, severe imaging findings)

Question 20

From which organs do brain metastases most often arise?

Answer 20

• lung (most common)
• breast
• bowel
• skin (melanoma)
• kidney

Question 21

Describe the imaging findings for the most common brain malignancy.

Answer 21

• glioma is the most common brain malignancy, of which astrocytoma is the most common subtype
• the biggest concern for glioma is that once symptomatic (‘a mild headache’), they are often too late for management
• grade 1: appears normal on MRI
• grade 2/3: solid tumour with central necrosis and a rim that enhances with contrast and surrounding oedema (‘ball’ shape)
• grade 4 (glioblastoma multiforme/GBM): crosses the midline (corpus callosum) - ‘butteflies’ or ‘gum on carpet’, meaning they are incredibly difficult to excise

Question 22

Describe the management of glioma and GBM.

Answer 22

• if low grade, glioma can be excised
• temozolamide (TMZ), a BBB-penetrant alkyating agent, is used first-line
• additional chemotherapy agents include carmustine wafes, bevacizumab (anti-VEGF), everolimus (mTOR inhibitor), and dabrafenib + trametinib (BRAF + MEK1/2 inhibitor)
• glioma is completely resistant to immunotherapy (‘cold’ tumour)

Question 23

Describe the Monroe-Kellie doctrine.

Answer 23

• the skull (calvaria) is composed of three components: blood (130ml), CSF (130ml), and brain (1300ml).
• the doctrine states the sum of the 3 components is constant, namely that an increase in one will cause a decrease in another or both

Question 24

Which factors or pathologies may lead to a raised ICP?

Answer 24

Three common clinical settings:
- generalised brain oedema (ischaemia, tumours, vascular obstruction etc.)
- increased CSF volume (hydrocephalus)
- focally expanding mass lesions (tumours, infarcts, haematomas, abscesses etc.)

[see flowchart on OneNote]

Question 25

Describe the pathology and management of cerebral oedema.

Answer 25

Two types of cerebral oedema: vasogenic and cytotoxic
- vasogenic: occurs due to disruption to the BBB, occuring most commonly due to tumours or abscesses (but may occur secondary to contusion or haemorrhage)
- cytotoxic: occurs due to cell death, secondary to TBI, haemorrhage, or ischaemia
- treatment with hypertonic saline and glucocorticoids (vasogenic oedema only)

BBB: blood brain barrier; TBI: traumatic brain injury

Question 26

Describe the congenital malformations that cause hydrocephalus.

Answer 26

• Chiari malformation: herniation of the cerebellar tonsils (vermis) through the foramen magnum. there are four main types, with type I being the most common. NB type II is also known as Arnold-Chiari malformation
• Dandy-Walker malformation: agenesis or hypoplasia of the cerebellar tonsils (vermis), which is replaced by an expanded fourth ventricle

Question 27

Describe the pathology, clinical features, investigation findings, and management of normal pressure hydrocephalus (NPH).

Answer 27

• enlarged lateral ventricles in elderly patients thought to arise secondary to reduced CSF absorption in the arachnoid villi (communicating hydrocephalus). these changes may occur after head injury, SAH, or meningitis
• clinical features: Hakim’s triad - urinary incontinence, dementia, and gait disturbance - often described as wet, wacky, and wobbly
• imaging reveals hydrocephalus with ventriculomegaly in the absence of (or out of proportion to) sulcal enlargement
• management is with ventriculoperitoneal shunting
• complications of Mx occur in 10% and include seizures, infection, and intracerebral haemorrhage

Question 28

Describe the risk factors, clinical features, and management of idiopathic intracranial hypertension (IIH).

Answer 28

• risk factors: obesity, female sex, pregnancy, and drugs (combined OCP, steroids, tetracyclines, retinoids/vitamin A, lithium)
• clinical features: headache, blurred vision, enlarged blind spot, CN VI palsy (a false localising sign)
• management:
  – weight loss (diet and exercise, but medications such as semaglitide and topiramate [also a carbonic anhydrase inhibitor] may be considered by specialists)
  – additional carbonic anhydrase inhibitors (e.g., acetazolamide)
  – repeated LP (temporary measure)
  – surgery: optic nerve sheath decompression and fenestration; ventriculoperitoneal shunt

Question 29

Why is raised ICP an absolute contraindication for lumbar puncture?

Answer 29

dramatically increased risk of brain herniation in cases of raised ICP

Question 30

Describe the clinical features of a raised ICP.

Answer 30

• headache
• cognitive impairment (reduced GCS)
• N&V
• papilloedema (bilateral optic nerve head swelling associated with raised ICP
• late signs: coma, fixed/dilated pupils, hemiplegia, hyperthermia, increased urinary output, Cushing triad (bradycardia, irregular respiration, widened pulse pressure)

Question 31

Describe the management of raised ICP.

Answer 31

• maintain CPP to prevent ischaemia or compression
• maintain the head in the midline, loosen ties/collars etc., avoid coughing/gagging, elevate head of bed to 30-45 degrees
• pharmacological measures: diuretics (mannitol, hypotonic saline, furosemide, urea), prophylactic AEDs, and a barbiturate coma (‘nuclear’ option)
• surgical decompression (e.g. removing mass lesions or diverting CSF via ventriculoperitoneal shunt)

CPP: cerebral perfusion pressure