Neuroimaging Techniques and Applications

Indications and Protocolling for Imaging

Indications:

  • Trauma – NECT
  • Stroke – NECT ± CTA/MRA/angiography if SAH
  • 1st seizure – To exclude intracranial tumour, infection or other acute process. NECT if patient is in immediate postictal state or residual neurologic deficit, otherwise enhanced CT/MR. If chronic/refractory then MR including high-resolution coronals of the medial temporal lobes and other clinically suspicious areas.
  • Infection and cancer – Enhanced MR better than enhanced CT
  • Headache – Severe acute -> NECT (SAH, acute hydrocephalus, enlarging mass); chronic with no neurological signs -> unenhanced MR; chronic with signs -> enhanced MR
  • Coma or acute confusional state – NECT for haemorrhage
  • Dementia – Noncontrast MR for frontal mass, hydrocephalus, small-vessel ischaemic change, small infarcts, other treatable abnormality. If MR negative, then likely Alzheimer’s disease.

Dual energy CT (DECT) uses low and high energy XRs without increasing dose. The high energy XRs (eg 190keV) is far from iodine k-edge, hence reduces the density of iodine (‘virtual non-contrast image). High keV also reduces bone bloom. Iodine maps can be calculated.

Skull x-ray for trauma – Only useful for documentation of fracture for medicolegal reasons.

Perfusion Scan – Reduced flow with meningitis, vasospasm, trauma, sickle cell disease, stroke.

  • Contrast enhanced CT (CTP) – Large rapid bolus (5-10mL/sec) during continuous scaning of single slice/block.
  • Contrast enhanced MR (MRP) – More difficult to determine MTT and CBV due to flow effects hence they are relative values: rCBV (or negative enhancement interval), rCBF (maximum slope of decrease), rMTT (mean time to enhance).
  • Xenon-133 – Inhalation of Xe with brain concentration related to brain blood flow; freely crosses the BBB. Risk of sedation, bronchospasm, respiratory depression.
  • Arterial spin labelling (ASL) MR – Inversion of spins in arterial protons and measured as they pass through the brain, freely crosses the BBB. Currently is technically difficult and can only images a small region.

Ultrasound

  • Neonatal – Indications include congenital brain abnormality, hydrocephalus, infection sequalae, prematurity and hypoxia. Via anterior fontanelle (open until 2yo, but difficult after 12-14/12). 5-7.5MHz with wide angle. Coronal (frontal horns, 3rd ventricle, trigone) and sagittal planes (midline, 10o through frontal and body lateral ventricles, 20o through temporal horns. Supplemental views in axial (via thin temporal squamous bone; 3rd ventricle, cortex, COW) or via posterior fontanelle, sutures or foramen magnum.
  • Transcranial Doppler – Through infratemporal fossa to evaluate MCA and ACA.

MRI

  • Brain screen – T1WI, T2WI, FLAIR, DWI with ADC, GRE, ± T1 post-Gad. Sedation usually reuired <6yo, but may not be needed in neonates. Heavily weighted T2 (long TR/echo time 3,000/120) for 1yo due to high water content. FLAIR improves detection of abnormal fluid in periventricular and peripheral regions, haemorrhage. Precontrast T1 enables differentiaon between eg haemorrhage and enhancement. Flow compensation with gradient-moment nulling reduces artifact from dural sinuses esp posterior fossa. Post-contrast Gad for localisation of specific neurologic finding, seizure, ?tumour, ?infection.
  • MRI pituitary
  • MRI spine
  • Functional MRI (fMRI) – see Magnetic Resonance Imaging]
  • MR Spectroscopy (MRS) – see Magnetic Resonance Imaging

Catheter angiogram – Gold standard used for ?vasculitis (CTA and MRA cannot rule this out), AVMs, equivocal CTA/MRA, complex aneurysms. Haemodynamically significant stenoses when >50-70%, <2mm residual lumen, ECA opacification causes ICA opacification.

Findings

Emergency CT checklist:

  • Midline structures not deviated
  • Symmetry
  • ‘Smile’ of quadrigeminal plate cistern, ‘pentagon’/’Jewish star’ of suprasellar cistern
  • 4th ventricle midline and symmetrical
  • Lateral ventricles not enlarged

Midline structures:

  • Suprasellar region – Sella turcica, pituitary gland, infundibulum, optic chiasm, anterior 3rd ventricle, mamillary bodies, anterior interhemispheric fissue, tip of basilar artery, PCAs, ACAs, carotid siphons, PComm, optic nerve and tracts.
  • Pineal region – Midbrain, tegmentum, aqueduct of Sylvius, pineal gland, superior cerebellar vermis, superior vermian cistern.
  • Craniocervical junction – Anterior arch C1, odontoid process, cervical occipital ligaments, clivus, cerebellar tonsils (</=5mm below anterior and posterior lips of foramen magnum), obex (above foramen magnum). Any soft tissue other than the cervico-medullary junction and a smal portion of the cerebellar tonsil in the foramen magnum is pathologic.

Lesion analysis:

  • Mass or atrophy:
    • Mass (space occupying lesion/SOL) – Displacement of structures, midline shift, sulcal and ventricular effacement/compression.
    • Atrophy – Widening of sulci, enlargement of ventricle. Ipsilateral shift is rare (even in complete hemispherectomy), except commonly seen in congenital hemiatrophy. If >65yo and normal cognitive function then age-appropriate cerebral atrophy; if demented then Alzheimer’s disease. Reversible atrophy is seen in dehydration (eg Addison’s disease) or starvation (eg anorexia nervosa, bulimia), occasionally alcoholism (accompanying nutritional deficiency).
  • Intra- or extra- axial:
    • Extra-axial masses include subdural/epidural haematoma, meningioma, schwannoma, dermoid/epidermoid cyst. Broad dural surface, widening of ipsilateral subarachnoid/CSF spaces, dura draped around lesion, cortical vessels displaced inwards, trapping of CSF, dural enhancement, most enhance homogeneously (meningioma, schwannoma), less oedema cf intra-axial lesions, grey-white interface preserved, ‘white matter buckling’ (inward compression with thinning of fronds cf thickened with oedema from intra-axial), dural tail, may cause reactive bony change. May be intradural (eg meningioma) or extradural (eg bone metastasis, displaces dura inwards but otherwise same features as intradural).
    • Intra-axial masses include metastases, haemorrhage, primary tumour, abscess. Surrounded by parenchyma, expands gyri, narrow sulci/CSF spaces, tends to enhance ring-like or irregularly, has more surrounding oedema than extra-axial masses, extends through white matter tracts, blurring of grey-white interface.
  • Single lesions imply primary cerebral disease; multiple imply systemic disease (metastases, emboli).
  • Grey and/or white matter involvement. Grey matter involved from infarct, trauma or encephalitis; acute if associated with mass effect, chronic if atrophic. Expansile white matter is likely oedema. Vasogenic oedema is exclusively white matter, from disturbed BBB (cerebral tumour, abscess, haematoma), is frondlike, progresses relatively slowly and persisting over time; if oedema > size of lesion tumour or abscess more likely than haematoma. Cytotoxic oedema (‘grey matter pattern’) is high T2/hypodense with grey matter involvement, from increased tissue water after response to cell death (infarct, trauma, encephalitis).
  • Distribution (if grey matter involved). Infarct is wedgeshaped in vascular distribution or borderzone/watershed between major vascular territories (if multiple watershed infarcts suspect global hypoperfusion from cardiac arrest). Pure anoxia from carbon monoxide poisoning or respiratory arrest is bilateral deep grey matter. Traumatic lesions in orbital frontal and frontal polar regions, temporal poles, occipital poles, contra-coup, path of penetrating missle, location of trauma. Herpex simplex encephalitis involves medial temporal lobes (adjacent to trigeminal ganglia) and orbital frontal regions (adjacent to olfactory bulbs) from spread from oral and nasal mucosa.
  • Enhancement means breakdown of the tight capillary junctions of the blood-brain barrier (BBB), and the process is biologically active. Blood brain barrier (BBB) has tight junctions between endothelial cells so no direct communication between capillary and ECF or neurons, except: choroid plexus of ventricles, pineal gland, pituitary gland, median eminence (swelling on tuber cinereum), subcommisural organ, subfornical organ, area postrema, organum vasculosum of lamina terminalis. Otherwise intraparenchymal enhancement is only seen in presence of inflammation, infarct, infection, neoplasm (increased enhancement correlates with higher grade astrocytoma) or trauma; due to unlocking of tight junctions, increased pinocytosis of contrast, endothelial fenetration or increased permeability of endothelial membrane. Non-neoplastic enhancement appears only in acute phase, resolving with time. Amount of enhancement depends on volume/type/timing of contrast used, size of intravascular space, lesion vascularity, permeability of lesion vessels, and size of extravascular lesional space.
  • Signal intensity or attenuation pattern:
    • High T1 – Protein, methaemoglobin (subacute haemorrhage), gadolinium, manganese, calcium, iron, bright blood (flow), fat, cholesterol, melanin.
    • Low T1 – Water, deoxyhaemoglobin (acute haemorrahge), haemosiderin (old haemorrhage), calcification, gas, fast flow, viscous protein, susceptibility artifact, low protein, air-bone interface.
    • High T2 – Water, oedema.
    • Low T2 – High protein, deoxyhaemoglobin, haemosiderin or intracellular methaemoglobin, melanin, calcium/calcification, gas, highly concentrated gadolinium, fast flow, fat, metal, susceptibility artifact, air-bone interface.
  • Tumour margin – Every glioma and almost every intra-axial tumour lacks a capsule, hence may migrate far, spreading through white-matter tracts.

Reaction to Injury

Inflammation in the CNS causes rubor (hyperperfusion), calor (heat), tumour (oedema), but no dolor (pain) unless meninges are affected. In most cases BBB is affected causing enhancement. Later there is neuronal death with gliosis and encephalomalacia. Reaction depends on cell type:

  • Neuronal injury
    • Acute injury (red neurons) – Cell death (necrosis or apoptosis). Red on H&E, cell body shrinks.
    • Subacute/chronic injury (degeneration) – Progressive disease. Cell loss (apoptosis) and reactive gliosis. Trans-synaptic degeneration when most of afferent input has been lost.
    • Axonal reaction – Damage to axons causes protein synthesis and axonal sprouting, enlarging cell body.
  • Astrocytes are metabolic buffers and detoxifiers, contribute to BBB, control flow of macromolecules. Gliosis/astrogliosis is hypertrophy and hyperplasia of astrocytes. Injury to astrocytes (hypoxia, hypoglycaemia, toxic) causes cytoplasmic swelling.
  • Oligodentrocytes and ependymal cells have limited reaction to injury.
  • Microglia (macrophage system of CNS) react with proliferation, aggregate in areas of necrosis (microglial nodules) and dying neurons. In inflammatory foci blood-derived macrophages are the principle phagocytic cells.

Cerebral parenchymal oedema is usually combination of vasogenic and cytotoxic oedema.

  • Vasogenic oedema – Disruption of BBB allowing shift of fluid from intravascular space. Localised (inflammation, tumour) or generalised.
  • Cytotoxic oedema – Increased intracellular fluid from neuronal, glial or endothelial cell membrane injury eg hypoxia/ischaemia, metabolic damage.
  • Interstitial/hydrocephalic oedema – Increased intraventricular pressure causes flow across the ependymal lining.