Neurosurgery Flashcards

1
Q

What can cause compression of the spinal cord?

A

Compression of the spinal cord can be due to:

  • Trauma
  • Non-traumatic causes:
    • Tumours - both primary and metastatic tumours
    • Infection - staphylococcal abscess, tuberculoma.
    • Prolapsed intervertebral disc (central).
    • Cyst: arachnoid, syringomyelia.
    • Haemorrhage.
    • Skeletal deformity: kyphoscoliosis, achondroplasia, spondylolisthesis.
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2
Q

Describe the presentation of cord compression

A
  • Back pain: is usually the first symptom. It often starts weeks before other features and becomes progressively unremitting, keeping the patient awake at night. There may also be thoracic dermatomal pain which is misinterpreted and leads to a long and unrewarding search for the cause of chest or abdominal pain.
  • Sensory symptoms: such as paraesthesiae or a sensation of limb heaviness or pulling, may then occur.
  • Sensory loss: may be apparent as a sensory level on testing. It is wise to test for pin-prick (spinothalamic function) and joint position sense/vibration sense (dorsal column function)—anterior or posterior portions of the cord may be selectively compressed.
  • Weakness: is often first described as clumsiness but soon progresses to clear loss of power.
  • Autonomic dysfunction: if the sympathetic pathways are involved, especially in high thoracic or cervical lesions, hypotension, bradycardia, or sometimes cardiac arrest may occur. This may be triggered by noxious stimuli such as pain, UTI, or abdominal distension caused by constipation or bladder outflow obstruction.
  • Sphincter dysfunction: commences as hesitancy or urgency of micturition and may progress to painless urinary retention with overflow. Constipation is another consequence of cord compression.
  • Respiratory failure: occurs with high cervical cord compression and is one cause of acute neuromuscular respiratory paralysis.

Fever should alert one to the possibility of an infectious cause.

Can also present as conus or cauda equina syndrome

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3
Q

What are the red flags / clinical features of cauda equina syndrome?

A

Cauda equina lesions present with LMN signs - leading to a flaccid, flexic, and often asymmetric paraparesis. Lumbosacral pain occurs early; bladder and bowel dysfunction appears relatively late. A sensory level is found in a saddle distribution up to L1 (corresponding to roots carried in the cauda equina). The red flags of cauda equina syndrome are:

  • Bilateral sciatica (raidculopthy of lumper nerve roots)
  • Progressive evolving neurology
  • Saddle anaesthesia (numbness over genitals and inner buttocks)
  • Urinary symptoms
  • Bowel symptoms
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4
Q

Describe the assessment and management of cord compression

A

A thorough neurological examination is important to localise the pathology (I.e. at what nerve root) and a history is important to determine the cause. A general examination is also very important - remember that a common cause is malignant compression from metastatic disease. Perform a careful examination, including the breasts, testicles, and thyroid if appropriate.

If spinal cord compression is a differential, organise an urgent MRI, CXR (? malignancy).

If the cause appears to be infective (fever, neutrophilia, raised CRP): send blood, sputum, and urine cultures.

Discuss the case with the regional neurosurgical centre, and consult a senior oncologist regarding advice for urgent radiotherapy for neoplastic disease and malignant compression. For non-malignant causes, patients should be treated with corticosteroids (bolus of dexamethasone IV).

  • Control pain and act to prevent constipation.
  • Urinary catheterization if there is bladder dysfunction.
  • Prophylactic SC heparin if immobile.
  • Monitor ABG and FVC in cases of high cervical compression or compromise.
  • Monitor haemodynamics and watch for autonomic dysfunction.
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5
Q

What is the aetiology of raised intracranial pressure (ICP)?

A

Causes of raised intracranial pressure:

  • Idiopathic intracranial hypertension
  • CNS inflammation, infection, and/or abscess
  • Space-occupying lesions
    • Intracranial haemorrhage or hematoma
    • Aneurysm
    • Intracranial tumours
  • Elevated venous pressure (e.g., as a result of heart failure)
  • Increased CSF (hydrocephalus)
  • Metabolic disturbances (e.g., hyponatremia, hepatic encephalopathy)
  • Epilepsy and seizures
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6
Q

What is the normal physiological intracranial pressure?

A

Physiological ICP is ≤ 15 mm Hg in adults (in supine position), children generally have a lower ICP

  • ICP varies with the relative position of the head towards the rest of the body and is influenced by certain physiological processes (e.g., cardiac contractions, sneezing, coughing, Valsalva maneuver).
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7
Q

What are the physiological consequences of raised intracranial pressure (ICP)?

A
  • Decreased cerebral perfusion pressure (CPP). CPP is the effective pressure that delivers blood to the cerebral tissue. CPP = mean arterial pressure - ICP. Therefore, if the ICP rises, the CPP diminishes (as long as the arterial pressure remains constant).
  • Herniation. As a bony structure, the skull is rigid and can not expand to compensate elevated internal pressure.
    • This may result in direct physical damage or in blocking of cerebral vessels and subsequent ischemia.
  • Cushing triad.
    • ↑ Intracranial pressure → decreased perfusion pressure within the brain → compensatory activation of the sympathetic nervous system to maintain cerebral perfusion → increase systolic blood pressure
    • This leads to stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia
  • ↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing (Cheyne Stokes style respiration).
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8
Q

What are the clinical features of raised intracranial pressure (ICP)?

A
  • Cushing’s triad: irregular breathing, widening pulse pressure and bradycardia
  • Reduced levels of consciousness
  • Headache
  • Vomiting
  • Papilloedema
  • Psychiatric changes

In infants: macrocephaly, bulging fontanel, sunset sign.

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9
Q

What are the investigations for raised intracranial pressure (ICP)?

A

CT/MRI: may indicate mass lesions, midline shift, or effacement of the basilar cisterns

Invasive ICP monitoring may be useful in patients who are at high risk of developing raised ICP, such as those with trauma or intracranial haemorrhage. Intraventricular monitors are the gold standard.

  • > 20 mmHg indicates elevated intracranial pressure that requires treatment
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10
Q

Describe the acute management of raised intracranial pressure (ICP)

A

To acutely reduce ICP:

  • Head elevation
  • Controlled hyperventilation. Cerebral blood flow is largely dependent on PaCO2. Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP.
  • IV mannitol

Patients also need:

  • Cardiopulmonary support
  • Sedation, analgesia, antipyretic therapy, antiseizure medication
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11
Q

Describe the post-acute management of raised intracranial pressure (ICP)

A

Goal of ICP management is generally to keep ICP < 20 mm Hg.

  • Positioning : e.g., head elevation (about 30 degrees), avoiding neck flexion/rotation or circumstances that may provoke Valsalva responses.
  • Fluid management: patients should be euvolemic, blood hypoosmolarity should be avoided
  • Hyperventilation: up to a pCO2 of 26–30 mm Hg
  • Hypothermia

Causal treatment (e.g., removal of brain tumor) if possible

Medical therapy - osmotic diuretics draw water out of the brain and into the blood from which it can be excreted in the urine:

  • IV mannitol: can generally be administered every 6–8 hours, effects last for up to 24 hours
  • IV hypertonic saline: particularly for short-term treatment

Removal of CSF via an intraventricular monitor with drainage system (e.g., external ventricular drain or lumbar drain) or a cerebral shunt (e.g., in hydrocephalus patients).

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12
Q

What is the definition and epidemiology of idiopathic intracranial hypertension?

A

Idiopathic intracranial hypertension (also known as pseudotumour cerebri and formerly benign intracranial hypertension) is a condition classically seen in young, overweight females characterised by chronically elevated intracranial pressure (ICP).

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13
Q

What are the clinical features of raised idiopathic intracranial hypertension?

A

Patients present with:

  • Diffuse headaches
  • Visual symptoms including blurred vision (due to papilloedema), photopsia (seeing flashes of light), diplopia and retrobulbar pain.
  • Pulsatile tinnitus

Also may present with sixth nerve palsy (abducens nerve) due to it being tethered as its exits the pons and inside Dorello’s canal.

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14
Q

What are the investigations for raised intracranial pressure (ICP)?

A

The following tests should always be performed:

  • Ophthalmologic examination which may show bilateral papilledema. Visual field test may show peripheral loss of vision
  • MRI to rule out other causes of increased ICP
  • Lumbar puncture: elevated opening pressure >20-25 cm H2O (with patient lying on the side, legs extended). Normal CSF analysis with no signs of inflammation or bleeding.
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15
Q

Describe the management of raised idiopathic intracranial hypertension

A
  • Weight loss
  • Medical (first-line):
    • Diuretics e.g. acetazolamide (carbonic anhydrase inhibitor)
    • Topiramate is also used, and has the added benefit of causing weight loss in most patients
  • Surgery:
    • Optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
    • A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
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16
Q

What is the aetiology and risk factors for a Subarachnoid Haemorrhage?

A
  • Rupture of a saccular ‘berry’ aneurysm (85%) at the base of the brain (usually at the circle of Willis). Conditions associated with berry aneurysms include PKD, Ehlers-Danlos syndrome and coarctation of the aorta.
  • Perimesencephalic haemorrhage
  • Arteriovenous malformations, coagulation disorders, vertebral or carotid artery dissection.

Risk factors include hypertension, smoking, family history, autosomal dominant polycystic kidney disease, and connective tissue disorders.

17
Q

What are the clinical features of a Subarachnoid Haemorrhage?

A

Patients present with a sudden onset severe headache (described as worst ever, or as if hit on the back of the head). Half of all patients present with loss of consciousness.

Patients also commonly present with nausea, vomiting, neck stiffness, and photophobia.

On Examination

There is evidence of meningism: neck stiffness, Kernig’s sign (resistance or pain on knee extension when hip is flexed) because of irritation of meninges with blood.

Glasgow Coma Scale: Assess and regularly monitor deterioration. Altered mental status is common.

There may be signs of increased intercranial pressure such as papilloedema, IV or III nerve palsy, hypertension and bradycardia.

Focal neurological deficits usually present the next day, and so is only uncommonly seen.

18
Q

What are the investigations for a Subarachnoid Haemorrhage?

A

If a SAH is suspected from history and examination, an emergency CT scan should be performed. It will show hyperdense areas in the basal cisterns, major fissures, sulci, and in severe cases the ventricular system.

CT scan is negative in 7% of cases. If CT scan does not show SAH, and if still highly suspected, perform a lumbar puncture test at least 12 hours after onset of symptoms (to allow development of red blood cell breakdown). It will show xanthochromia (result of red cell breakdown).

Referral to neurosurgery to be made as soon as SAH is confirmed. At the same time, bloods should be taken to look at:

  • FBC
  • Clotting profile - coagulopathy may be present
  • U&Es - hyponatraemia may occur due to salt wasting
  • Troponin - elevated in around 25% of cases, without an MI.

After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:

  • CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
  • +/- digital subtraction angiogram (catheter angiogram)
19
Q

Describe the management of a Subarachnoid Haemorrhage

A

Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon.

Until the aneurysm is treated, the patient should be kept on strict bed rest, well-controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm

  • Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature)
  • Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt.
20
Q

What is the definition and epidemiology of cervical myelopathy?

A

Myelopathies are neurological disorders due to compression of the spinal cord. Myelopathies can be cervical, thoracic, or lumbar.

  • Cervical myelopathy is the most common type of myelopathy in adults above 55 years of age.
21
Q

What is the aetiology of cervical myelopathy?

A

Causes for compression of the spinal cord include:

  • Blunt or penetrating trauma (e.g., fracture, epidural hematoma)
  • Infection (e.g., abscess)
  • Radiation therapy
  • Autoimmune disorders (e.g., rheumatoid arthritis, neuromyelitis optica)
  • Neoplasms (e.g., meningiomas, nerve sheath tumors, metastases) or cysts (e.g., epidermoid cysts)
  • Ossification of the posterior longitudinal ligament (OPLL)
  • Congenital narrowing of the cervical spinal canal
  • Degenerative diseases
    • Spinal stenosis
    • Ankylosing spondylitis
    • Discogenic myelopathy (central disc herniation)
    • Multiple sclerosis
22
Q

What are the clinical features of cervical myelopathy?

A

Features depend on the level of compression and the onset may be sudden (e.g., with trauma), step-wise, or slowly progressive (e.g., degenerative diseases).

  • Neck, shoulder, upper limb, or lower limb pain (neck stiffness may be present)
  • Signs and symptoms of lower motor neuron lesions at the level of the lesion (e.g., weakness and atrophy in the arms and/or hands in lesions of the thoracic spine)
  • Signs and symptoms of an upper motor neuron lesion below the level of the lesion (e.g., abnormal spastic gait is often an early sign; hyperreflexia or a positive Babinski’s sign may be present)
  • Impaired sensation (e.g., numbness, impaired proprioception, ataxia)
  • Impaired bladder and bowel control
23
Q

What is the best investigation for cervical myelopathy?

A

MRI of the spine determines the site of narrowing of the medulla and the underlying pathology

Myelography (possibly with CT): when MRI is contraindicated

24
Q

Describe the management of degenerative cervical myelopathy

A

All patients with degenerative cervical myelopathy should be urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery). This is due to the importance of early treatment. The timing of surgery is important, as any existing spinal cord damage can be permanent.

  • Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery but at present, most patients are presenting too late. In one study, patients averaged over 5 appointments before diagnosis, representing >2 years.

Currently, decompressive surgery is the only effective treatment. It has been shown to prevent disease progression. Close observation is an option for mild stable disease, but anything progressive or more severe requires surgery to prevent further deterioration.

Physiotherapy should only be initiated by specialist services, as manipulation can cause more spinal cord damage.