DWI hyperintensityIn addition to cerebral infarction, what else do you know!!

Among a series of diseases in neurology, the most common DWI hyperintensity is naturally the acute phase of ischemic stroke, which I am afraid that everyone who studies medicine knows, but when you see diffuse DWI hyperintensity that mainly involves the cortex and is not distributed according to the blood supply area of the brain, you often need to think of one of the most terrible diseases in neurology: CJD, Creutzfeldt–Jakob disease
。 Recently, the author has encountered two such patients in the clinic, one is a proposed CJD, which basically means a "death sentence", 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 hyperintensity.

encephalitis

Encephalitis (including viral encephalitis, autoimmune encephalitis, etc.
) may have DWI hyperintensity
involving the cortex/subcortex.
Encephalitis is generally not difficult to identify, acute onset, fever, headache and other symptoms
.
Encephalitis involving the cortex will have seizures, psychiatric symptoms, etc.
, and lumbar puncture to check cerebrospinal fluid routine, biochemical, viral antibodies, autoimmune encephalitis antibodies, etc.
can help diagnose, Figure 1 is the magnetic resonance examination results
of patients with monoherpes encephalitis 6 days after onset.

Figure 1 Herpes encephalitis, 6 days onset, temporal lobe lesions on both sides can be seen, especially on the right, T2WI, FLAIR, DWI are all high signal, ADC figure is low signal

Epilepsy-mediated changes in brain imaging

For patients with a clear history of seizures, epilepsy-mediated brain imaging changes need to be considered, unlike the etiology of epilepsy (tumor, FCD, etc.
), epilepsy-mediated brain imaging changes are often reversible, most of them show T2WI hyperintensity on magnetic resonance, about half show DWI hyperintensity, common sites of involvement include cortical/subcortical, basal ganglia, white matter, corpus callosum, cerebellum, and there are no other specific clinical manifestations, as shown
in Figure 2.
Figure 2 Results of two cranial MRs in a 42-year-old woman with prolonged subclinical status epilepticus
.
A is T2WI, B, C, F is DWI, D is ADC diagram, E and G are FLAIR, it can be seen that at 4 days of onset, obvious DWI hyperintensity lesions can be seen in bilateral parietal-occipital lobes, T2 phase is also high intensity, ADC is low intensity, and the lesions disappear at 25 days of onset

Creutzko's disease

Creutzfeldt–Jakob disease (CJD) is a class of infectious, progressively deteriorating neurodegenerative diseases caused by prion viruses, mainly manifested as progressive dementia, mental disorders, myoclonus, etc
.
Specific three-phase waves can be seen on EEG later in the course of the disease, and some patients are positive
for cerebrospinal fluid 14-3-3 protein.
There is currently 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 image abnormalities in the early stage of CJD, and some imaging abnormalities often appear in the middle and late stages, more typical are cortical ribbon (also known as streamer sign, characterized by cortical DWI hyperintensity, common in sporadic CJD), hockey-stick sign (refers to the symmetrical involvement of bilateral thalamic occipital and dorsomedial thalamus T2, DWI hyperintense lesions, common in variant CJD).

。 Clinically, patients with progressive dementia, vertebral body/extravertebral symptoms, and EEG abnormalities (three-phase waves) often point to CJD
if they present with lace signs.
Figure 3 shows the results
of a magnetic resonance examination in a patient with sporadic CJD.
Figure 3 Lace sign (streamer sign), patient with sporadic CJD, A and B are DWI, C is ADC diagram, and D is FLAIR
.
The patient's bilateral cortical asymmetric DWI hyperintensity (arrows), basal ganglia DWI hyperintensity (triangular arrows), low signal on the ADC plot of the lesion, and high intensity on FLAIR can be seen

Mitochondrial encephalomyopathies with hyperlactic acidemia and stroke-like seizures

Mitochondrial encephalomyopathies are a complex group of diseases involving multiple systems with extensive biochemical and genetic defects
.
Mitochondrial encephalomyopathies with hyperlactemia and stroke-like seizures (MELAS) are a relatively well-studied class of mitochondrial encephalomyopathies
.
Stroke-like seizures are the dominant 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 present clinically with 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 the cortex and subcortical white matter, and deep white matter is not affected, showing T2WI, DWI hyperintensity similar to stroke-like presentation
.
Magnetic resonance spectroscopy can detect the presence of lactic acid in infarcts and other unaffected areas of
the brain.
A typical magnetic resonance presentation is shown
in Figure 4.

Figure 4 MELAS patient, A is DWI, cortical/subcortical DWI hyperintensity, B is ADC figure, lesion low intensity, C is FLAIR, lesion hyperintensity, D is chronic phase FLAIR, lesions are almost disappeared, and the affected part of the brain tissue is atrophy

Diffuse cerebral ischemia - hypoxic changes

The DWI and ADC plots are the sequences showing the best signaling of early ischemia-hypoxic brain tissue (better than T2WI and FLAIR), with significant DWI hyperintensity and ADC low-signal changes in the early stages, most commonly occurring in the cortex/subcortical of the watershed region, and often involving the basal ganglia
.
A clear 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 hyperintensity

other

Other disorders can alter cortical/subcortical DWI hyperintensity, such as posterior reversible encephalopathy syndrome (PRES), hemiplegic migraine, moyamoya disease, etc
.

Looking back here, the diseases involving the cortex / subcortex are mainly 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 several others are not difficult to identify through other clinical data, if necessary, MELAS can be magnetic resonance spectroscopy, genetic testing, etc.
, CJD needs to complete electroencephalogram, cerebrospinal fluid 14-3-3 protein test
.

Introduction to the principles of DWI

Figure 1 Dispersion restriction principle

The T2 projection effect is due to the high signal of DWI caused by the extension of T2, while the ADC value does not decrease
.
Thus, hyperintense lesions on DWI may reflect a strong T2 transmission effect rather than a true diffusion reduction (Figure 2).

Common diseases with 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

Fig.
3 MRI findings of cerebral infarction (2 hours of 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 infarction zone, smaller ADC value, high signal in DWI, and low signal on ADC plot
.
DWI high signal
can be displayed within 30 minutes at the earliest.
Over time, the DWI signal gradually decreases
.

Brain abscess

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

Fig.
4 Comparison of ring-shaped strengthening lesions

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

The patient with the left figure had significantly high DWI intensity, and the ADC figure was low intense, which was a brain abscess; The patient on the right has low DWI signal, and the ADC figure is high signal, which is a brain tumor
.

Fig.
5 Ring reinforcement comparison (brain abscess versus glioblastoma)

Brain abscess is mainly a hematogenous infection, with the frontal and parietal lobes being the most common, and the posterior fossa is less than 15%, mostly located at the gray-white matter junction
.
It is generally single, and it is rare (immunosuppressed state is more common).

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

Smoothness of the wall of the abscess: purulent>tuberculous>fungal.

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

Fig.
6 Brain abscess (limited diffusion)

Clinically, brain abscesses are sometimes difficult to distinguish from diseases such as metastases, and the key points of differentiation can be found in Table 2
.

Brain tumors

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

High-grade gliomas (including anaplastic glioma, anaplastic oligodendroglioma, glioblastoma, etc.
), lymphoma, metastases, medulloblastoma, central nervous cell tumor, primitive neuroectodermal tumor PNET and other brain tumors, usually manifested as DWI high signal, low ADC value
.

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

For gliomas, low-grade gliomas have slightly lower cell densities and equal or slightly higher DWI signals, while high-grade gliomas have higher cell densities, high DWI signals, and reduced ADC values
.
This is not absolute, because the DWI high signal also contains the T2 signal, so some tumor DWI high signal sections contain both ADC low signal (diffusion-limited portion) and equal/high signal (part of T2 projection effect).

Typical radiographic findings of different brain tumors

Fig.
7 Hairy 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 hyperintensity, ADC decrease)

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

Fig.
12 Meloblastoma (high DWI, low ADC)

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

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

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