What is dwi mri

The first problem is that the term "diffusion-weighted imaging" is used to denote a number of different things:. Additionally, confusion also exists in how to refer to abnormal restricted diffusion.

This largely stems from the initial popularisation of DWI in stroke, which presented infarcted tissue as high signal on isotropic maps and described it merely as "restricted diffusion", implying that the rest of the brain did not demonstrate restricted diffusion, which is clearly not true. Unfortunately, this shorthand is appealing and is more widespread than using the more accurate but clumsier "diffusion demonstrates greater restriction than one would expect for this tissue.

To make matters worse, many are not aware of the concept of T2 shine-through , a cause of artifactual high signal on isotropic maps, or interpret it as a binary feature with T2 contribution to signal either present or absent when in reality there is always a T2 component even to regions with true T2 diffusion restriction.

A much safer and more accurate way of referring to diffusion restriction is to remember that we are referring to actual apparent diffusion coefficient ADC values, and to use wording such as "the region demonstrates abnormally low ADC values abnormal diffusion restriction " or even "high signal on isotropic images DWI is confirmed by ADC maps to represent abnormal restricted diffusion".

As opposed to essentially free diffusion of water kept inside a container, diffusion of water inside brain tissue, for example, is hindered primarily by cell membrane boundaries. The overall diffusion characteristics of a single volume represent the combined water diffusion in a number of compartments:.

The contribution of each one of these will depend on the tissue and pathology. For example, in acute cerebral infarction it is believed that the decrease in ADC values is the result of a combination of water moving into the intracellular compartment where its diffusion is more impeded by organelles than it is in the extracellular space and the resulting cellular swelling narrowing the extracellular space 6. Similar mechanisms result in low ADC values in highly cellular tumors e.

The further an individual water molecule diffuses during the sequence the more it will be exposed to varying gradient strength and the more it will be dephased reducing the amount of signal returned. This occurs at a much smaller scale than a single voxel.

The strength of this effect in other words how much the signal will be attenuated by diffusion is determined by the b value. A variety of techniques for generating diffusion maps have been developed. The more easily water can diffuse i. For example, water within cerebrospinal fluid CSF can diffuse very easily, so very little signal remains and the ventricles appear black. Next, the ease with which water can diffuse is assessed in various directions; the minimum is 3 orthogonal directions X, Y and Z and we will use this for the rest of this explanation.

This is done by applying a strong gradient symmetrically on either side of the degree pulse. The degree of diffusion weighting is dependent primarily on the area under the diffusion gradients which is in turn related to the amplitude and duration of the gradient and on the interval between the gradients.

The combination of these factors generates the b value. The higher the number the more pronounced the diffusion-related signal attenuation. Stationary water molecules acquire phase information by the application of the first gradient. After the degree pulse, however, they are exposed to the exact same gradient because they have not changed location which undoes all the effects of the first since they have flipped degrees. Hence at the time the echo is generated they have retained their signal.

Moving water molecules, on the other hand, acquire phase information by the first gradient but as they are moving when they are exposed to the second gradient they are not in the same location and thus are not exposed to precisely the same gradient after the degree pulse. Hence they are not rephased and they lose some of their signal.

The further they are able to move the less successfully they will be rephased and the less signal will remain. These images can then be combined arithmetically to generate maps that are devoid of directional information isotropic : isotropic diffusion-weighted images what we usually refer to as DWI and ADC maps. To generate the isotropic DWI maps, the geometric mean of the direction-specific images is calculated. These can either be calculated directly from the isotropic DWI images or by finding the arithmetic mean of ADC values generated from each directional diffusion map.

Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Updating… Please wait. Thrombolytic or endovascular therapies are the treatment options for acute stroke. Selection of patients eligible for these therapies is critical to achieve good outcomes and avoid fatal complications. Both time from stroke symptom onset to treatment and the individual therapeutic time window secondary to variations in collateral circulation determine the long-term functional outcome after stroke.

Therefore, imaging—including DWI—has great prognostic value and is crucial to treatment decision making because it allows early diagnosis and an estimation of both the time of onset and the infarct-salvageable brain proportion. Despite some technical challenges need for strong gradients, the size of the spinal cord, flow artefacts , DWI is useful in assessing cord ischaemia.

Although signal changes were reported on both T2 and DWI in the majority of cases, DWI showed a clear benefit over conventional MRI in some patients, in whom T2 failed to identify an abnormality [ 19 , 20 ]. According to Thurnher et al. Spinal cord ischaemia.

High T2 signal abnormality in the conus medullaris with diffusion restriction on DWI arrows compatible with an ischaemic lesion. The new definition of TIA is based on a biological concept tissue injury. A TIA is characterised by a transient episode of neurological impairment caused by focal ischaemia without acute infarction [ 23 ].

Therefore, whether a symptomatic ischaemic episode will result in ischaemic infarction cannot be based solely on time duration. If MRI shows areas of restricted diffusion in a patient whose symptoms have resolved and lasted less than 24 h, the term cerebral infarction with transient symptoms is preferred [ 25 ].

Once a morphological change has been demonstrated on imaging, the risk of full-blown stroke is higher, and treatment should be more aggressive. It consists of an eccentric rim of hyperintensity surrounding the hypointense arterial lumen on MRI. It has traditionally been described on T1-weighted fat-saturation MRI sequences [ 26 ], but may be seen on other sequences such as diffusion-weighted imaging Fig.

Arterial dissection. The signal intensity of intramural haematoma in arterial dissection is influenced by the paramagnetic effects of blood breakdown products [ 27 ]. The haematoma is isointense on T1WI and shows T2 prolongation a few hours after bleeding has occurred in the hyperacute phase oxyhaemoglobin phase.

The T2 signal becomes hypointense in the acute stage deoxyhaemoglobin phase. T1 and T2 signals become hyperintense in the subacute phase, between 7 days and 2 months methaemoglobin phase. In cerebral venous thrombosis, hyperintensity on DWI has been suggested to represent restricted proton movement within the clot, but it is also observed within the dissected vertebral artery wall in the hyperacute and early subacute phases [ 28 ].

DWI can therefore be useful in the diagnosis of acute dissection, when the intramural haematoma can barely be detected on fat-saturated T1-weighted images because of obscuration of its isointense signal by the surrounding soft tissues with similar signal intensity. DWI using EPI usually shows susceptibility artefacts at the air-tissue or bone-soft tissue interfaces.

Artefacts present as a fuzzy linear hyperintensity or diffuse hypointensity, which are usually easy to differentiate from the focal round or linear well-demarcated hyperintensity typical of intramural haematoma [ 28 ]. Correlation with T1- or T2-weighted images is also helpful. The use of an SE sequence, reducing the echo time and increasing the acquisition matrix, may be helpful to minimise these susceptibility artefacts. Ischaemia in the setting of venous thrombosis has a different physiology from arterial infarction [ 29 ].

Therefore, diffusion imaging helps to define the stage of the disease because it allows differentiation between irreversible venous infarction DWI hyperintense with restricted diffusion and reversible venous oedema DWI isointense with increased diffusion. In contradistinction to arterial stroke, DWI-positive venous stroke may be completely reversible.

In venous ischaemia, DWI may be able to show the actual thrombus as increased signal intensity [ 30 ] because of the restricted movement of water molecules within the venous clot Fig. However, sinus thrombosis may have different appearances depending on the stage of thrombus formation, which has been demonstrated by ex vivo MRI measurements [ 31 ].

Venous thrombosis. DWI a , ADC map b and sagittal reconstruction of T1 3D with gadolinium c show thrombosis of the left jugular vein arrows , presenting with restricted diffusion and a filling defect in the vessel after contrast administration. Taking into account that venous infarctions have a higher tendency to bleed, and haemorrhage can also restrict diffusion, imaging features in venous infarction may be considerably variable, depending on the time after onset and the sequence of events.

In the cases where DWI is positive, this may indicate the earliest sign of non-reversibility due to progression to cytotoxic oedema and therefore the possibility of permanent infarction or haemorrhagic transformation. Regarding extraaxial tumours, DWI allows distinction between epidermoid and arachnoid cysts. Epidermoid cysts show diffusion restriction, as opposed to arachnoid cysts, which follow CSF signal intensity on all sequences.

In meningiomas it has been shown that ADC values correlate with tumour cellularity [ 35 ] but this has not been found to provide any additional value in differentiating histopathological subtypes of meningiomas [ 36 ].

Concerning glial tumours, quantitative assessment with DWI has mainly targeted an estimation of cellularity based on its inverse relation with water diffusivity in the extracellular compartment. Hence, ADC can be considered as a tumour biomarker in gliomas: the higher the tumour grade, the lower the mean tumour ADC values [ 37 ]. However, the range of ADC values within a given glioma varies markedly [ 38 ] and there is an overlap between ADCs of grade II astrocytomas and glioblastomas, probably due to the inherent tissue heterogeneity associated with gliomas across different grades, limiting the use of DWI.

Despite this, in the context of low-grade tumour follow-up and where appropriate, a decrease in the ADC value could be considered an early sign of tumour progression.

Another use of DWI on imaging of CNS tumours is to aid in the distinction between glioblastoma and primary CNS lymphoma, two entities with markedly different treatment strategies and not always easy to differentiate with conventional imaging in patients presenting with an enhancing brain mass. There are some published works aiming to find an ADC threshold for differentiating lymphoma from other tumours [ 40 ] Fig. Guzman et al. Primary CNS lymphoma. Left frontal periventricular lesion showing prominent diffusion restriction, presenting with hyperintensity on DWI a , low ADC value b and mild hyperintensity on T2WI c , all typical features of this type of hypercellular tumour.

T1WI post gadolinium d shows homogeneous and intense contrast enhancement. Attempts to differentiate glioblastoma from metastasis based on the FA values of the surrounding oedema have been made [ 42 ] based on the assumption that glioblastoma has a tendency to grow in an infiltrative manner typically invading surrounding tissues.

Conversely, metastatic tumours tend to grow in an expansive manner and typically displace the surrounding brain tissues rather than invading them [ 43 ]. Another entity associated with brain tumours is intracranial hypertension, which can be seen as papilloedema, bright on DWI [ 44 ]. DTI and tractography reconstruction can be helpful for surgical planning in patients with brain or spinal cord masses.

It shows white matter tracts as well as displacement or interruption of these tracts secondary to different pathologies. Slow-growing tumours displace the fibres surrounding the lesion, whereas in ischaemia or trauma, representing more acute insults, the fibres are usually interrupted [ 45 ] Fig. DTI for surgical planning. Patient with an ependymoma in the lower cervical spinal cord with areas of high T2 signal a and enhancement after gadolinium administration b.

DTI shows displacement of the fibres c , which is usually consistent with a slow-growing lesion. An additional important use of DWI after surgical resection of a tumour is to detect areas of diffusion restriction in the cavity margins on MRI performed in the first 48 h, corresponding to small postsurgical infarctions.

The importance of this imaging time window lies in the fact that the majority of these infarcts will enhance after 1 or 2 weeks and could be potentially interpreted as residual tumour or tumour progression Fig.

Post-surgical ischaemia. Immediate follow-up MRI in a patient who underwent surgery for resection of a suspicious enhancing mass. In the medial aspect of the resection cavity asterisk there is an enhancing area on the T1 post-contrast sequence c , arrow. This finding alone could represent residual tumour, but the presence of restricted diffusion with high signal on DWI a and a low ADC value b meant that a small area of peri-surgical ischaemia was more likely.

Three-month follow-up T1 post-gadolinium MRI d shows absence of enhancement in the same region arrowhead , confirming this diagnosis. Regarding paediatric tumours, DWI can non-invasively add valuable information that can be used to narrow the differential diagnosis of the three most common tumours of the posterior fossa in children medulloblastoma, ependymoma, pilocytic astrocytoma.

Several studies have demonstrated that ADC values in the enhancing, non-necrotic, non-oedematous, solid parts of cerebellar tumours are negatively correlated with tumour grade [ 46 ] high-grade tumours such as medulloblastoma are characterised by high cellularity, low extracellular space, and cells with large nuclei and high nuclear-to-cytoplasmatic ratios, causing decreased diffusion.

An even greater accuracy can be achieved by combining DWI and MRS to obtain more information about the tumour proliferative potential [ 48 ]. DWI has also been reported to be useful in detecting relapse of embryonal tumours such as medulloblastoma, being more sensitive than contrast-enhanced MRI in subjects with the classic variant [ 49 ].

Abscesses of the brain can be bacterial, parasitic or fungal in origin. The appearance of bacterial abscesses on conventional imaging varies with the stage of abscess formation, but the typical features of the early capsule stage ring-enhancing lesion with a T2 hypointense rim and variable degree of associated vasogenic oedema can be similar to primary cystic or necrotic tumours Fig.

However, pyogenic abscesses show restricted diffusion with markedly decreased signal on the ADC map and elevated fractional anisotropy FA within the abscess cavity [ 50 ] because of the presence of intact inflammatory cells and bacteria.

These impede the microscopic motion of water molecules, which helps to narrow the differential diagnosis of ring-enhancing lesions exceptions exist: metastases with high cellularity and haemorrhagic metastasis. Left parieto-occipital lesion with peripheral vasogenic oedema. DWI and ADC a and b , respectively show a clear area of increased diffusion within the core, corresponding to a necrotic centre. On T1 3D post gadolinium the mass shows ring enhancement. Subacute haematoma.

Right parietal mass arrowhead showing diffusion restriction within the core on DWI and ADC maps a and b , respectively and a ring-enhancing pattern on T1 post gadolinium c. This was a subacute haematoma. Clinical context is important to differentiate haemorrhage from abscess. There is also a subacute ischaemic lesion in the inferior right frontal lobe arrows that shows early pseudonormalisation of the ADC and gyriform enhancement post gadolinium.

Reddi et al. A study [ 52 ] has shown that the abscess cavity had lower ADC and higher FA compared with the cystic cavity of glioblastomas and metastases, possibly representing high viscosity and organised viable inflammatory cells.

In addition, FA values were higher in the enhancing rim of the abscess than in glioblastoma and metastasis, maybe because of the presence of concentric layers of collagen fibres. Regarding the peritumoral zone of oedema, this study showed that the presence of a hyperintense FA rim with lower FA values was much more frequent in glioblastomas and metastases than in abscesses. This suggests that microstructural changes in the oedematous white matter immediately surrounding the abscess may be different from those surrounding glioblastoma and metastasis, possibly because of acute versus longer time to formation, respectively.

Right occipital mass showing marked diffusion restriction within the core on DWI and ADC maps a and b , respectively and a peripheral enhancing pattern on T1 post gadolinium c. DWI helps to differentiate ring-enhancing lesions because restricted diffusion in the centre of the mass is characteristic of pyogenic abscesses. In this case, diffusion-based sequences also helped to identify ventriculitis arrows.

Fungal abscesses can have either restricted or elevated diffusion in the centre depending on the content , in opposition to pyogenic and tuberculous abscesses that typically show restricted diffusion in the core of the cavity [ 53 ].

Aspergillus CNS infections tend to be haemorrhagic, which is an additional cause of restricted diffusion. In general, it is important to include fungal abscesses in the differential diagnosis in immunocompromised patients because of different targeted antifungal treatment. Parasitic abscesses may also show both restricted and elevated diffusion [ 54 ]. For example, cysticercosis cysts have a similar or slightly increased DWI signal to CSF, and the scolex may be seen as a hyperintense focus inside [ 55 ].

In toxoplasmosis, diffusion restriction is highly variable possibly overlapping with lymphoma characteristics, its main differential diagnosis [ 56 , 57 ]. In cerebral malaria, DWI is useful in detecting areas of brain infarction [ 58 ].

In the postsurgical setting, the accuracy of DWI in the diagnosis of CNS infectious complications is low, showing a high false-negative rate. The absence of restricted diffusion is not sufficient to exclude the presence of pyogenic postcraniotomy infection and should not be used as the main determinant in patient management in this clinical setting [ 59 ]. Diffusion restriction is commonly seen in viral encephalitis, and the location of the affected area may guide the radiologist in the identification of the infectious agent.

For example, the limbic system medial temporal and inferior frontal cortex is the typical involved area in herpes simplex encephalitis. Viruses more frequently causing potentially reversible lesions in the splenium of the corpus callosum are the influenza virus [ 60 ], Epstein-Barr virus, HHV-6 and papovirus JC [ 61 ]. Thalamic involvement is typically seen with the West Nile virus [ 62 ], Japanese encephalitis or Eastern equine encephalitis. DWI may help detect lesions earlier than conventional MR imaging.

In patients diagnosed with West Nile virus encephalitis, diffusion restriction with no FLAIR or T2 signal abnormalities has been reported to be a sign of good prognosis [ 63 ]. Progressive multifocal leukoencephalopathy PML is secondary to the infection of oligodendrocytes by the JC polyoma virus, which typically remains latent until reactivation in the context of an immunocompromised state HIV, natalizumab or other immunosuppressive treatments.

Due to its ability to investigate white matter architecture and diseases, DWI shows regions of active infection and cell swelling with high signal and allows distinction of two parts in the lesions: a central core whose size can correlate to the clinical status and disease duration and a peripheral rim which includes a heterogeneous component and areas of surrounding cytotoxic oedema with low ADC and areas of vasogenic oedema and glial repair with intermediate ADC [ 64 ].

DWI MR has high diagnostic accuracy and is the most sensitive neuroimaging technique for striatal and cortical lesions from an early stage [ 65 ]. Typically, diffusion-weighted hyperintensity is progressive and persistent over many weeks, affecting the striatum and cortex.

DWI hyperintensity may resolve late in the disease. In multiple sclerosis, the majority of active plaques show normal or increased diffusivity, but some may show restricted diffusion, often at the margins [ 68 ]. It is important to bear this in mind since, in the appropriate context, these plaques can mimic a lacunar infarct. Possible explanations for the decreased ADC in active plaques are decreased extracellular space due to myelin oedema or cytotoxic oedema and decreased water movement in the extracellular space secondary to inflammation [ 15 ].

DTI demonstrates different degrees of mean diffusivity increase and FA decrease in T2-hyperintense established lesions or even before their formation. These changes are also present in normal-appearing white or grey matter of patients with MS [ 69 ] as opposed to ADEM, which shows normal diffusivity within normal-appearing white matter.

Diffusivity changes in MS correlate with areas of demyelination and axonal loss in postmortem studies [ 70 ]. Diagnosis is based on electroencephalography EEG , lumbar puncture and serological testing for appropriate biomarkers presence of autoantibodies, lymphocytic pleocytosis or oligoclonal bands in CSF.

Neuroimaging should be performed despite yielding a high proportion of false negatives in autoimmune encephalitis more than in paraneoplastic encephalitis syndromes [ 71 ]. When positive, the studies are usually non-specific high FLAIR signal in cortical or subcortical regions—hippocampus, basal ganglia, white matter. Diffusion restriction may be present in the areas showing abnormal signal. Although limbic encephalitis has been known as a paraneoplastic syndrome, there have been recognised forms characterised by serum autoantibodies, directed against glutamic acid decarboxylase anti-GAD and voltage-gated potassium channels VGKC , not related to neoplastic conditions.

On DTI studies, a reduction of fractional anisotropy and increased mean diffusivity have been shown in the white matter of patients suffering from NMDAR encephalitis the most common type of autoimmune encephalitis , suggesting that white matter damage is a contributor to the pathophysiology and clinical phenotype, even correlating with disease severity [ 72 ].

Another study aiming to assess white matter integrity in the two forms of non-paraneoplastic limbic encephalitis characterised by serum autoantibodies GAD and VGKC concluded that GAD-limbic encephalitis presented with FA reduction, probably reflecting demyelination, whereas VGKC-limbic encephalitis caused no changes in the diffusion properties of white matter, probably because this condition is more limited to grey matter [ 73 ].

Abnormal signal intensity of the optic nerve due to diffusion restriction may be seen in ischaemic or traumatic optic neuropathy [ 74 , 75 ]. DWI has been suggested as a useful tool in differentiating these aetiologies from acute optic neuritis presumed autoimmune aetiology [ 76 , 77 ], where there is increased diffusivity in demyelinating plaques, related to disruption of myelinated axons, and decreased fractional anisotropy.

However, this should be interpreted in the clinical context, since optic neuritis may also show transient decreased diffusion in the acute phase Fig. Optic neuritis. High DWI signal a and low ADC value b representing restricted diffusion in the right optic nerve in a patient with non-specific optic neuritis.

With the exception of the orbital apex region, DTI of the optic nerve is facilitated by its anatomy and antero-posterior orientation. This can be useful in assessing tumours such as neurofibromas, schwannomas or meningiomas [ 78 ] as well as in brain malformations such as septo-optic dysplasia or optic nerve hypoplasia [ 79 ]. Other cranial nerves can also be studied with high-resolution DTI in some clinical situations.

Demonstration of atrophy or loss of anisotropy in cases of trigeminal neuralgia and fibre displacement in vestibulocochlear schwannomas are examples of this [ 80 ]. The DWI and DTI techniques allow quantitative analysis of microstructural changes in neurodegenerative diseases, even when no abnormalities are seen on conventional MRI sequences, because they are able to identify changes in brain tissue integrity.

These changes are characterised by a decrease in the number of barriers that restrict the movement of water, thus causing ADC to increase in brain areas where neurodegeneration occurs. This has led to an increase in the use of DWI in the diagnostic investigation of neurodegenerative parkinsonian syndromes. DWI has also highlighted the involvement of new areas in the pathophysiology of this condition, such as the optic radiations and middle cerebellar peduncles [ 84 ].

Diffusion-weighted sequences currently play a central role in neuroimaging. The already widespread qualitative assessment allowed by these sequences improves sensitivity in the depiction of several central nervous system conditions, whereas new models of diffusion sequences provide quantitative parameters, allowing potential biomarkers for diagnosis, prognosis and follow-up. The future of DWI will undoubtedly include technical improvements to enhance data fidelity, to achieve high isotropic resolution e.

Furthermore, advances in ultrahigh field technology are already being applied to DWI. Radiology 2 — Article PubMed Google Scholar. J Magn Reson Imaging 46 3 — Acad Radiol 21 4 — Neuroradiology 57 10 Liney GP, Holloway L, Al Harthi TM et al Quantitative evaluation of diffusion-weighted imaging techniques for the purposes of radiotherapy planning in the prostate.

Br J Radiol 88 Radiologia 59 4 — Magn Reson Med 14 2 — Magn Reson Med 18 1 — Neurology 45 1 — PubMed Google Scholar. Stroke 46 1 — Venkatesan R, Lin W, Gurleyik K et al Absolute measurements of water content using magnetic resonance imaging: preliminary findings in an in vivo focal ischemic rat model. Magn Reson Med 43 1 — Lancet Neurol 10 11 — Dietemann J-L Neuro-imagerie diagnostique. Elsevier Masson. Stroke 30 11 — Stroke 43 11 — Stroke 44 5 — Eur Radiol 14 11 — Neuroradiology 45 8 — Neuroradiology 48 11 — The American academy of neurology affirms the value of this statement as an educational tool for neurologists.

Stroke 40 6 — Stroke 44 7 — Ann Neurol 57 5 —