DWI hyperintensity is not necessarily cerebral infarction

Among a series of diseases in neurology, the most common DWI hyperintensity is naturally the acute phase of ischemic stroke, which is probably known to medical students, but when you see diffuse DWI hyperintensity that mainly involves the cortex and is not distributed according to the blood supply area of the cerebral blood vessels, you often need to think of one of the most terrible diseases in neurology: Creutzfeldt–Jakob disease
。 Recently, the author has encountered two such patients in the clinic, one is a proposed diagnosis of CJD, which basically means pronouncing the "death penalty", and the other has not yet been diagnosed, so I specially reviewed with you several types of diseases
that are mainly manifested as cortical / subcortical DWI high intensity.

encephalitis

Encephalitis (including viral encephalitis, autoimmune encephalitis, etc.
) may present with cortical/subcortical DWI hyperintensity
.
Encephalitis is generally not difficult to identify, acute onset, fever, headache and other symptoms
.
Encephalitis involving the cortex will cause seizures, psychiatric symptoms, etc.
, and lumbar puncture examination cerebrospinal fluid routine, biochemistry, viral antibodies, autoimmune encephalitis antibodies, etc.
can help diagnose, Figure 1 is the results
of magnetic resonance examination in patients with herpes simplex encephalitis at 6 days of onset.

Figure 1 Herpes simplex encephalitis, 6 days of onset, visible temporal lobe lesions on both sides, especially on the right, T2WI, FLAIR, DWI are all high-intensity, ADC figure is low-signal

Epilepsy-mediated brain imaging changes

For patients with a clear history of seizures, epilepsy-mediated brain imaging changes need to be considered, unlike the etiology of epilepsy (tumors, FCDs, etc.
), epilepsy-mediated brain imaging changes are often reversible, most of the MRI is T2WI hyperintensity, about half of which are DWI hyperintensive, common sites of involvement include cortex/subcortical, basal ganglia, white matter, corpus callosum, cerebellum, and clinically there are no other specific findings, as shown
in Figure 2.
Figure 2 Two head MR results
in a 42-year-old woman with prolonged subclinical status epilepticus.
A is T2WI, B, C, F is DWI, D is the ADC graph, E, G is FLAIR, it can be seen that at 4 days of onset, bilateral parietal occipital lobes can be seen with obvious DWI high-intensity lesions, T2 phase is also high-intensive, ADC is low-signal, and the lesion disappears at 25 days of onset

Creutzkot-Jakoh

Creutzfeldt–Jakob disease (CJD, Creutzfeldt–Jakob disease) is an infectious and progressively deteriorating neurodegenerative disease caused by prion viruses, mainly manifested as progressive dementia, mental disorders, myoclonus, etc
.
Later in the course of the disease, EEG showed specific triphasic waves, and some patients were positive for
CSF 14-3-3 protein.
So far, there is no effective treatment for this disease, and patients generally die
within six months to two years after the onset of clinical symptoms.
There are no imaging abnormalities in the early stage of CJD, and some imaging abnormalities often occur in the middle and late stages, the more typical are the lace sign (cortical ribbon, also known as streamer sign, characterized by cortical DWI hyperintensity, common in sporadic CJD), hockey-stick sign (refers to T2, DWI hyperintense lesions with symmetric involvement of bilateral thalamic occipital and dorsomedial thalamus, common in variant CJD).

。 Clinically, lace signs often point to CJD
in patients with progressive dementia, vertebral/extravertebral symptoms, and abnormal EEG (triphasic waves).
Figure 3 shows the results
of a magnetic resonance examination in a patient with sporadic CJD.

Figure 3 Lace sign (streamer sign), in patients with sporadic CJD, A and B are DWI, C is ADC diagram, and D is FLAIR
.
The patient's bilateral cortical asymmetry DWI hyperintensity (arrow), basal ganglia DWI hyperintensity (triangular arrow), low signal on the lesion ADC plot, and high signal on FLAIR can be seen

Mitochondrial encephalomyopathy with hyperlactic acidemia and stroke-like attacks

Mitochondriary encephalomyopathies are a complex group of diseases involving multiple systems, with extensive biochemical and genetic defects
.
Mitochondrial encephalomyopathy with hyperlactic acidemia and stroke-like seizures (MELAS) is a relatively well-studied type of mitochondrial encephalomyopathies
.
Stroke-like onset is the main clinical feature of
MELAS.
Although MELAS stroke-like episodes often recover quickly and completely early in the course of the disease, the patient's neurological status continues to deteriorate
once the first stroke-like episode occurs.
Stroke-like seizures can be clinically manifested by a variety of neurologic symptoms such as seizures, headache, altered mental status, focal weakness, decreased vision, sensory loss, dysarthria, and ataxia.

Typical MELAS magnetic resonance lesions are mostly distributed in cortical and subcortical white matter, and deep white matter is not involved, and appears as T2WI, DWI hyperintensity, stroke-like findings
.
Magnetic resonance spectroscopy detects the presence of lactic acid in infarcts and other unaffected areas of
the brain.
A typical magnetic resonance performance is shown in
Figure 4.

Figure 4 In patients with MELAS, A is DWI, visible cortical/subcortical DWI hyperintensity, B is ADC plot, visible lesion hypointensity, C is FLAIR, visible lesion hyperintensity, D is the patient's chronic phase FLAIR, visible lesions almost disappear, affected part of the brain tissue atrophy

Diffuse cerebral ischemia - hypoxic changes

DWI and ADC plots are the best sequences showing early ischemia-hypoxic brain tissue signal alterations (better than T2WI and FLAIR), with significant DWI hyperintensity and ADC hyposignal alterations in the early stage, most commonly occurring in the cortex/subcortex in the watershed region and often involving the basal ganglia area
.
A well-established history of diffuse cerebral ischemia and hypoxia, such as cardiac arrest, is not difficult to diagnose
.
Figure 5 shows a typical image representation
.
Figure 5 Patients with cardiac arrest, diffuse cerebral ischemia-hypoxia changes, A~D is DWI, E~H is FLAIR, diffuse bilateral cortical hyperintensities can be seen

other

There are also some diseases that can cause cortical/subcortical DWI high-intensity changes, such as reversible posterior encephalopathy syndrome (PRES), hemiplegic migraine, moyamoya disease, etc
.

To review here, diseases involving the cortex / subcortex are mainly as described above, many of which require patients to have a clear history support, such as epilepsy / status epilepticus, cerebral ischemia - hypoxia, migraine history, etc.
, and the other several are not difficult to identify through other clinical data, if necessary, MELAS can perform magnetic resonance spectroscopy, genetic examination, etc.
, CJD needs to improve EEG, cerebrospinal fluid 14-3-3 protein examination
.

Introduction to DWI principle

In order to understand the concept of DWI, it is essential to understand free diffusion and diffusion limitations
within the cellular microenvironment.
In 1827, when Brown used a microscope to observe pollen particles suspended in water, he found that the pollen particles were constantly moving
irregularly in the water.
The constant random motion of free water molecules, known as Brownian motion
.
Instead, the movement of water molecules within the cellular microenvironment is hindered
by interactions between cell compartments.

The DWI sequence is the sequence
in which the molecules of reacting water are freely diffused.
There are two main reasons for DWI high signal, one is that true dispersion is limited and its ADC value is reduced; The other is a high signal that diffuses unlimited, and its ADC value does not decrease, mainly because of the T2 projection effect
.
The main causes of diffusion restriction include three types: one is cytotoxic edema, the other is increased cell density, and the third is the viscosity
of the fluid.

Fig.
1 Dispersion limited principle

The T2 projection effect is a high signal of DWI due to the extension of T2 without a decrease
in the ADC value.
Therefore, high-intensity lesions on DWI may reflect strong T2 transmission effects rather than true diffusion reduction (Figure 2).

Common diseases of DWI hyperintensity include cerebral infarction, brain abscess, brain tumor, demyelinating disease, metabolic toxic disease, CJD, etc
.

Fig.
2 T2 transmission effect (35-year-old woman, multiple sclerosis)

Cerebral infarction

DWI sequence is the mainstay of examination for
diagnosing cerebral infarction.
In the first few minutes of cerebral infarction, brain tissue energy metabolism is disrupted, Na-K+/ATPase and other ion pumps fail, so that the ions inside and outside the cell are out of balance, and a large amount of extracellular water enters the cell, forming cytotoxic edema
.
The water content of the entire infarct area did not increase, but the water content inside and outside the cells changed
.

At this time, T2WI, T1WI, and FLAIR can not show the lesion, only DWI that can show the diffuse movement of water molecules can show the lesion
.

Fig.
3 MRI manifestations of cerebral infarction (2 hours after onset)

Cytotoxic edema, increased intracellular water molecules, causing cell swelling, resulting in smaller extracellular space, reduced extracellular water molecules, distortion and deformation of extracellular space, decreased diffusion movement of water molecules in the infarcted area, smaller ADC value, DWI displayed as high signal, ADC plot displayed as low signal
.
DWI high signals
can be displayed as early as 30 minutes.
Over time, the DWI signal gradually decreases
.

Brain abscess

I'll put two ring-reinforced pictures first, you can guess which is a brain abscess and which is a brain tumor
.

Fig.
4 Comparison of ring intensified lesions

DWI is a good means to
distinguish brain abscess from high-grade gliomas and metastases.
For the two cases in the figure above, in fact, if you add a DWI sequence, it is easy to distinguish.

The DWI of the patient on the left is obviously high-intensity, and the ADC is low-intensive, which is a brain abscess; The DWI low signal of the patient on the right and the high signal of the ADC figure are brain tumors
.

Fig.
5 Ring intensification contrast (brain abscess versus glioblastoma)

Brain abscess is mainly hematogenous infection, the frontal and parietal lobes are the most common, the posterior cranial fossa is less than 15%, mostly located at the
gray-white matter junction.
Generally, it is single, and it is rare to occur more often (immunosuppressive states are more common).

Pus manifests as long T1 long T2, FLAIR low signal, DWI high signal, ADC low signal; The pus wall contains fibrous components, T1 is equal/slightly higher signal, T2 is equal/slightly lower signal, and the uniform annular strengthening (smoother, deep thin, shallow thick); There may be daughter foci (satellite foci) that rupture to form small abscesses
.

Degree of smoothness of the abscess walls: purulent> tuberculous> fungal
.

DWI uniformity: purulent, tuberculous is more uniform, fungal is less uniform
.

Fig.
6 Brain abscess (limited diffusion)

Clinically, brain abscess is sometimes difficult to distinguish from metastases and other diseases, and the main points of differentiation can be seen in Table 2
.

Brain tumors

The DWI signal of brain tumors depends mainly on the ADC value (cell density) and T2 signal
.
Low ADC values reflect high cell density and reduced extracellular space; High ADC values reflect low cell density, low nucleus-toplasm ratio, and increased extracellular matrix (Figure 9).

High-grade gliomas (including anaplastic gliomas, anaplastic oligodendrogliomas, glioblastomas, etc.
), lymphomas, metastases, medulloblastomas, central neurocytomas, primitive neuroectodermal tumors PNET and other brain tumors, usually manifested as DWI high signal, low ADC value
.

Relative ADC values: lymphoma< high-grade glioma< metastases<b10>.

For gliomas, low-grade gliomas have a slightly lower cell density and have equal or slightly higher DWI signals, while high-grade gliomas have higher cell density and high DWI and reduced
ADC values.
This is not absolute, because DWI high signal also contains T2 signal, therefore, some tumors DWI high signal part contains both ADC low signal (diffusion-limited part) and iso/high signal (part of T2 projection effect).

Typical radiographic findings of different brain tumors

Fig.
7 Hair cell astrocytoma (DWI and other signals)

Fig.
8 Low-grade oligodendroglioma (high DWI, high ADC)

Fig.
9 Glioblastoma (high DWI, low ADC)

Fig.
10 Lung cancer brain metastasis (DWI high signal, ADC decreased)

Fig.
11 Lymphoma (dense tumor cells, high DWI, low ADC)

Fig.
12 Medulloblastoma (high DWI, low ADC)

Fig.
13 Central nervous cell tumor (dense tumor cells, high DWI, low ADC)

Fig.
14 Original neuroectodermal tumor PNET (high DWI, low ADC)