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Neurology 3rd year > Neurosurgery > Flashcards

Neurosurgery Flashcards

1
Q

What is a radiculopathy?

A

The site of injury in radiculopathy is at the level of the spinal nerve root. The result is pain (known as radicular pain), weakness in limbs, numbness/parasthesia, and difficulty in controlling specific muscles
People sometimes refer to radiculopathy as having a “pinched nerve.”

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2
Q

Radiculopathy - Most affected levels?

A

L5/S1 + L4/5 levels most affected

also cervical spine

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3
Q

Lumbar radiculopathy

A

Sciatica
Pain in the lower back and hip radiating down the back of the thigh into the leg. Damage from L1 to S1 caused by compression of the nerve roots which exit the spine.

-possible causes: heavy lifting, trauma eg car accident, tumour, diabetes

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4
Q

Back pain - differentials

A

 Lumbar muscular strain/sprain (MSK pain)
 Herniated nucleus pulposus
 Spinal stenosis
 Compression fracture
 Degenerative disk disease or facet arthropathy
 Sacroiliitis
 Spondylolysis and/or spondylolisthesis

Abdo referred pain: Pancreatitis, Pyelonephritis, Renal colic, Peptic ulcer disease

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5
Q

Disc degeneration - clinical features

A

persistent low back pain (worsens with axial loading (standing or sitting) and improves with recumbence)
radicular leg pain
activity-related symptoms

can progress to disc prolapse

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6
Q

Spinal stenosis

A

Lumbar spondylosis refers to degenerative conditions of the lumbar spine that narrow the spinal canal, lateral recesses, and neural foramina.

activity-related back pain
leg pain when walking (Neurogenic claudication) -pain and weakness in the thighs and calves and a sensation of numbness in the lower extremities. Sitting is better than standing and patients may find it easier to walk uphill rather than downhill.
stooped posture when walking
leg numbness or paresthesias

Dx: MRI
Tx: laminectomy

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7
Q

What is the cauda equina?

A
  • bundle of spinal nerves from L2 to L5, all 5 sacral nerves, and the coccygeal nerve
  • ## the spinal cord stops growing in infancy at the level of L3, at birth. By about 12 months of age, it reaches its permanent position at the level of L1 or L2
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8
Q

What level is a LP performed?

A

level L3/L4, or L4/L5, where there is no risk of accidental injury to the spinal cord

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9
Q

Cauda equina syndrome?

A
  • surgical emergency
  • nerve roots in the lumbar spine are compressed, disrupting sensation and movement.
  • It can lead to permanent paralysis, impaired bladder and/or bowel control, loss of sexual sensation, severe back pain, saddle anaesthesia, absent ankle reflexes
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10
Q

Cauda equina syndrome - causes

A
  • trauma (eg Cx of LP, burst fractures, disc herniation)
  • spinal stenosis
  • Paget disease, neurosarcoidosis, chronic inflammatory demyelinating polyneuropathy, ankylosing spondylitis
  • osteomyelitis
  • tumour
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11
Q

Cauda equina syndrome - management

A

surgical decompression: laminectomy or removal of bone fragments/tumour/herniated disc etc.

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12
Q

How to distinguish infarction and haemorrhage on CT?

A
  • infarction = hypodense lesion (dark grey)

- haemorrhage = hyperdense (light grey or white)

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13
Q

SAH - features

A
  • The most common cause of SAH is trauma, however they may also be spontaneous (typically aneurysms).
  • RF: hypertension, smoking, positive family history, and autosomal dominant polycystic kidney disease
  • Sudden onset severe occipital headache (‘worst ever’), “thunderclap” (starts and intensifies quickly) with nausea and photophobia, loss of consciousness/coma/seizures
  • CT = Blood (hyperdense - bright) is seen within the CSF spaces - in the basal cisterns, fissures and sulci
  • LP used to confirm SAH if CT is -ve. LP is performed > 12h following the onset to allow the development of xanthochromia (result of RBC breakdown)
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14
Q

SAH - management

A

Referral to neurosurgery to be made as soon as SAH is confirmed

  • cardiopulmonary support (ICU)
  • aneurysm: open surgical clipping or endovascular coil embolisation (interventional neuroradiologists)
  • prophylaxis: CBB (nimodipine) to lower BP +/- anticonvulsant (eg phenytoin) +/- stool softener (prevent straining) +smoking cessation
  • Hydrocephalus (if present) is treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt
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15
Q

Cerebral Arterivenous Malformations (AVM) - definition

A

Congenital lesions of direct connections between cerebral arteries and veins. The two most common presentations of AVMs are intracerebral haemorrhage (50%-70% of cases) and seizures (approximately 20%).

  • development of ‘arterialised’ veins with proliferation of smooth muscle and elastin in the vessel wall.
  • local arterial hypotension and venous hypertension (oedema)
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16
Q

Cerebral AVM - presentation and treatment

A 
Presentation:
sudden-onset focal neurological deficit
seizures
reduced conscious level
Treatment:
- conservative = eg manage seizures
- sometimes surgical = craniotomy + AVM ablation
17
Q

Intracerebral haemorrhage - features

A
  • RF: HTN, vascular lesions, brain tumour, stroke with thrombolysis
  • History of HTN, sudden onset severe posterior headache, dysphasia and vomiting, right hemiparesis
  • CT = areas of white lesions (haemorrhage) and sorrounding low density/dark (oedema)
  • treatment usually conservative, unless there is a big clot with impaired consciousness which requires surgical evacuation
18
Q

2ary prevention of intracerebral haemorrhage

A
  • BP control (labetalol or nicardipine)
  • lifestyle = well-controlled diabetes, good nutrition and exercise, and abstinence from smoking, use of illegal drugs, or heavy drinking
19
Q

Extradural haematoma - features

A
  • ~70% occur in temporoparietal region
  • ~75% associated with ipsilateral fracture
  • Usually middle meningeal artery at pterion (temple)
  • CT = dense (white) biconvex blood collection
  • “lucid interval”: immediately following the trauma and a delay before symptoms become evident - rapid decline in consciousness
  • may press on CN 3 = ipsilateral fixed and dilated pupil, eye will be positioned down and out
  • contralateral weakness of the extremities and contralatetral loss of visual field
20
Q

Extradural haematoma - management

A
  • supportive: iv fluids, intubation
  • surgical: hematoma is evacuated through a craniotomy or emergency burr hole
  • treat high ICP = raising the head of the bed to 30°, osmotic diuresis with hyperosmotic saline solution
  • prophylactic antiepileptics up to 7 days (Levetiracetam or phenytoin)
21
Q

Subdural haematoma - features

A
  • RF: trauma, coagulopathy, anticoagulant use, >65 years
  • less commonly rupture of aneurysm of AVM
  • typically caused by high-speed injuries or acceleration-deceleration injuries, or blow to the side of the head
  • CT = dense (white) semi-lunar blood collection
  • headache, N+V, diminished eye response, diminished verbal response, diminished motor response, confusion
22
Q

When is surgery for a subdural haematoma not required?

A

1) Glasgow Coma Scale (GCS) score 9 to 15; subdural haematoma <10 mm; and midline shift <5 mm
2) GCS <9, stable between injury and emergency department; haematoma <10 mm; midline shift <5 mm; pupils reactive and symmetrical; and intracranial pressure <20 mmHg.

23
Q

Subdural haematoma - management

A

surgery if ≥10 mm size or midline shift >5 mm or neurological dysfunction: decompressive craniotomy or burr hole or durotomy and removal of clot

  • prophylactic AED as in extradural
  • correction of coagulopathy
  • intracranial pressure-lowering regimen as in extradural
24
Q

What is the normal range of ICP?

A

at rest, normally 7–15 mmHg for a supine adult

25
Q

What is hydrocephalus?

A

Abnormal dilatation of the cerebral ventricular system
due to accumulation of cerebrospinal fluid (CSF) causing increased pressure inside the skull.
- Older people may have headaches, double vision, poor balance, urinary incontinence, personality changes, or mental impairment.
- In babies, it may be seen as a rapid increase in head size

26
Q

Non-communicating Hydrocephalus

A

Ventricular dilatation caused by intraventricular obstruction. Causes:

  • Intraventricular Tumor
  • Extraventricular tumour : Pituitary adenoma, craniopharyngioma, medulloblastoma, meningioma
  • Ventriculitis
  • Haemorrhage: fresh clot, or adhesive arachnoiditis
  • acqueduct of sylvius stenosis
27
Q

Communicating Hydrocephalus

A

There is free flow throughout the ventricular system.
Impaired CSF resorption by the arachnoid granulation accounts for majority of cases
- SAH
Infectious meningitis
Malignant meningitis
Granulomatous meningitis : TB , sarcoidosis
Altered venous Dynamics : Vein of Galen malformation, venous obstruction

28
Q

Normal Pressure Hydrocephalus

A 
Reversible cause of dementia
A classical triad of features is seen
- urinary incontinence
- dementia and bradyphrenia
- gait abnormality (may be similar to Parkinson's disease)

Also known as idiopathic normal pressure hydrocephalus (INPH), is a condition with clinical features of hydrocephalus (i.e., levodopa-unresponsive gait apraxia), but without significantly elevated CSF pressure as measured by LP

Ix: hydrocephalus with an enlarged fourth ventricle
Tx: ventriculoperitoneal shunting

29
Q

Idiopathic Intracranial Hypertension

A
  • young, fat, female, weight gain, sleep apnoea, pregnancy,
  • reduced CSF absorption and increased ICP
  • headaches, pulse-synchronous tinnitus, transient visual obscurations, papilloedema, visual loss, neck and back pain, and diplopia.
  • Mx: weight loss, diuretics e.g. acetazolamide, repeated lumbar puncture, lumboperitoneal or ventriculoperitoneal shunt
30
Q

Hydrocephalus - management

A
  • short-term relief: external ventricular drain (ETV), also known as an extraventricular drain or ventriculostomy
  • long term: cerebral shunt - catheter into ventricles and drain into peritoneum (ventriculoperitoneal shunt) or right atrium (ventriculoatrial shunt) or pleural cavity (ventriculopleural shunt) or gallbladder
31
Q

Monro Kellie Doctrine

A

cranial constituents = BLOOD, BRAIN TISSUE and CSF

the cranial compartment is inelastic and the volume inside the cranium is fixed. The cranium and its constituents create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another

Neurology 3rd year (13 decks)

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