Mednotes

L11 Nervous System Neuroimaging

Properties2
tagsnervoussystem, lecture
aliasesL11 Nervous System Neuroimaging

10 min read

Overview

An introduction to imaging the nervous system: what each modality detects, how findings look, and when to choose one over another. It moves from the largely obsolete plain skull film, through CT (its physics, windowing and reconstructions, and the appearances of infarct, intraparenchymal haemorrhage, the extradural/subdural/subarachnoid compartments and tumour), to MRI (proton physics, T1 vs T2, FLAIR, DWI/ADC, angiography and spectroscopy), and closes with the practical comparison of CT against MRI and MRI’s contraindications.

Plain skull film

A plain skull X-ray shows the bony skull (parietal, frontal, temporal, zygomatic bones, mandible, asterion, external acoustic meatus, mastoid process, styloid process, posterior border of the ramus). It is very little used in modern medicine.

CT: how it works and how images are handled

  • CT uses an X-ray source and a detector array rotating around the patient to build a stack of cross-sectional slices.
  • Detection is by ionising radiation using a Geiger-type detector: a thin window, a rarefied gas fill and an electronic counter.
  • Cerebral haemorrhage appears white on CT because of the density of iron and protein in haemoglobin.
  • Image manipulation: CT data can be rendered as 3D reconstructions and colour coded, for example colour 3D reconstructions of the pelvis showing fracture sites in a patient who fell 3 m from a cement mixer onto concrete with suspected sacroiliac joint injury or pelvic fracture.
  • Windowing: the same axial data can be reconstructed as a soft tissue window (grey soft tissue detail, dark air spaces) or a bone window (bright, high-contrast bone).
  • Plane reconstruction: axial CT data can be reconstructed into other planes, for example sagittal, in either soft tissue or bone windowing.

CT appearance of cerebral infarction

  • An infarct is low density (dark) on the pre-contrast CT, for example a right middle cerebral artery infarct in the right hemisphere.
  • The three CT signs of the resulting oedema in a right MCA territory infarct:
    • Parenchymal hypodensity
    • Sulci effaced (flattened)
    • Grey/white differentiation lost

Intraparenchymal haemorrhage

Density changes with age of the bleed:

  • White (hyperdense) if recent, due to iron and protein in haemoglobin.
  • Dark (hypodense) if more than 1 month, as haemoglobin is resorbed leaving serum.

Possible causes: trauma, underlying tumour, vascular malformation, hypertensive bleed.

Vessels, dura and the haemorrhage compartments

The relevant spaces and structures around the brain are the dural sinus and the extradural, subdural and subarachnoid spaces, lying between skull, dura and brain surface.

Extradural haemorrhage

  • Caused by traumatic rupture of the middle meningeal artery, typically with a linear skull fracture.
  • Note the associated contra coup injury: petechial (pinpoint) haemorrhages on the opposite side, for example a right extradural haemorrhage with a left temporal lobe contra coup bleed.
  • The haematoma compresses and distorts the brain; clot can be seen exposed on the skull base.
  • Look for gas bubbles, which indicate a skull base fracture.
  • A large extradural haemorrhage can cause brain swelling with midline shift away from the side of the bleed (for example a left extradural haemorrhage shifting the midline to the right).
  • Assess with both soft tissue and bone windows to show the bleed and the associated fracture, and in axial, coronal and sagittal planes.

Subdural haemorrhage

  • Acute subdural haemorrhages appear as collections along the brain surface and may be bilateral.
  • Chronic subdural haematoma contains dark fluid blood, is encased in a membrane beneath the dura, and compresses and distorts the brain with deviation of the ventricles.
  • A right chronic subdural haematoma may be accompanied by cerebral atrophy, seen as a wide subarachnoid space.

Subarachnoid haemorrhage

  • Caused by a leaking aneurysm, for example an anterior communicating artery aneurysm on the circle of Willis; CT shows blood at the skull base.
  • CT angiography can reveal the culprit aneurysm (an anterior cerebral artery aneurysm in the example case).
  • The circle of Willis may be incomplete in a given patient.

Brain tumours on CT

Most brain tumours are low density on CT and then show contrast enhancement. A glioma imaged pre and post IV iodine contrast demonstrates this pattern.

MRI physics

The four steps of image generation:

  1. Hydrogen protons in tissue water, randomly oriented.
  2. The body is placed in the magnet (1.5 Tesla), aligning the protons.
  3. A radio pulse is applied at right angles to the magnetic field, exciting the protons.
  4. A radio signal comes out and is detected.

Scanner components: radio frequency coil, gradient coils, magnet, patient table.

Relaxation, following excitation of the magnetisation vector from the longitudinal (Z) axis into the transverse (XY) plane:

  • T2 is the rate of loss of transverse magnetisation.
  • T1 is the rate of recovery of longitudinal magnetisation.

MRI sequences

  • T1: water dark, with or without gadolinium contrast; anatomy sensitive.
  • T2: water white; fluid sensitive.
  • FLAIR (fluid attenuated inversion recovery): usually used for multiple sclerosis.
  • DWI (diffusion weighted imaging) plus the ADC (apparent diffusion coefficient) map, a logarithmic measure of diffusion.

Applying MRI to disease

Infarction

  • Acute right MCA territory infarction: loss of sulci on CT, with the infarct appearing hyperintense on T2 MRI one day later.
  • Mechanism of the DWI signal in acute cerebral infarction: interruption of cerebral blood flow causes rapid (within minutes) breakdown of energy metabolism and ion exchange pumps, leading to a massive shift of water from the extracellular into the intracellular compartment (cytotoxic oedema), producing a typical high-intensity area on DWI.
  • In a 77-year-old with a stroke 3 hours earlier, DWI shows the acute infarct as bright before it is visible on T2 or FLAIR.

Multiple sclerosis

T2 FLAIR MRI shows bright periventricular plaques of white matter demyelination.

Lateral medullary syndrome

T2 MRI shows infarction of the left side of the brainstem and cerebellum, presenting with left-sided ataxia, usually due to obstruction of the posterior inferior cerebellar artery (PICA).

Vascular imaging

  • Conventional arteriogram: a common carotid arteriogram performed by passing a catheter from the femoral artery to the neck, used to show a blocked internal carotid artery. Branches of the external carotid circulation are labelled on the image (superficial temporal, occipital, maxillary, facial, external carotid).
  • MRI angiography: MRI with IV gadolinium contrast and computer reconstruction of the vessels. In acute right middle cerebral artery infarction it shows a narrow right middle cerebral artery.

Glioma on MRI

  • A patient who drove a car at slow speed into a hedge and was vacant and confused at the scene was scanned for possible infarct or bleed; the CT was normal (“nad”). MRI (non-contrast T1, post-contrast T1, T2) showed a temporal mass lesion that enhanced with contrast: a glioma, a malignant brain tumour.
  • The lesion can be characterised further with T2, DWI and the ADC map.
  • MR spectroscopy of the tumour shows a choline peak, reflecting cell wall breakdown, and also a creatinine peak, with metabolite ratios (Cho, Cr, NAA and their ratios) reported alongside a colour metabolite map over the region of interest.

Important

A normal CT does not exclude a brain tumour: in the glioma case above the CT was unremarkable and the diagnosis was made on MRI.

Choosing between CT and MRI

CT is preferable over MRI in:

  • Acute trauma, head or body
  • The unstable patient

Time to perform: CT 5 seconds versus MRI 30 minutes.

MRI contraindications, a patient with:

  • Pacemaker
  • Metallic foreign body in a critical area, such as the orbit, or an intracranial aneurysm clip
  • Cochlear implants
  • Heart valves
  • Claustrophobia

Self-test

  1. Explain why an acute cerebral haemorrhage appears white on CT, and predict how its density changes after more than a month.
  2. List the three CT signs of oedema described in a right middle cerebral artery territory infarct.
  3. List the four possible causes of intraparenchymal haemorrhage given in the lecture.
  4. Describe the mechanism and vessel involved in an extradural haemorrhage, and state what a “contra coup” injury means here.
  5. On a CT of a head injury, what finding should prompt you to suspect a skull base fracture?
  6. Distinguish the CT and anatomical features of a chronic subdural haematoma from those of an extradural haemorrhage.
  7. A patient has subarachnoid blood at the skull base on CT. What underlying lesion is illustrated, and what investigation identifies it?
  8. Describe the four steps by which an MRI image is generated.
  9. Distinguish T1 from T2 in terms of what each measures and how water and anatomy appear on each.
  10. Explain why an acute infarct is bright on DWI within hours, before T2 or FLAIR change.
  11. What sequence is usually used for multiple sclerosis, and what does it show?
  12. Describe the clinical and imaging features of lateral medullary syndrome and the artery usually obstructed.
  13. State two situations in which CT is preferable to MRI, and give the scan times for each modality.
  14. List five contraindications to MRI.
  15. What peak on MR spectroscopy suggests a glioma, and what does it represent?
  16. Integrative: a patient becomes vacant and confused after a low-speed car crash and the CT is normal. Explain how you would proceed with imaging and what findings would support a diagnosis of glioma.

Answers

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