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    Home > Active Ingredient News > Study of Nervous System > Seeing DWI High Signal: These 5 Diseases Can't Be Ignored

    Seeing DWI High Signal: These 5 Diseases Can't Be Ignored

    • Last Update: 2022-04-24
    • Source: Internet
    • Author: User
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    ,DWI ,,、 DWI ,: (CJD, Creutzfeldt–Jakob disease)
    。, CJD,「」,, /DWI
    。 

    Among a series of diseases in neurology, the most common DWI high signal is naturally ischemic stroke and acute phase stroke .
    I am afraid that medical students know this, but when you see the main involvement of the cortex, and the blood supply area is not according to the cerebral blood vessels.
    When distributed diffuse DWI hyperintensity, one of the most feared diseases in neurology often needs to be thought of: Creutzfeldt–Jakob disease (CJD)


    .


    encephalitisencephalitis 

    Encephalitis (including viral encephalitis, autoimmune encephalitis, etc.


    ) may have DWI hyperintensity involving the cortex/subcortex


    Encephalitis (including viral encephalitis, autoimmune encephalitis, etc.


    Figure 1 Herpes simplex encephalitis, 6 days after onset, lesions in both temporal lobes can be seen, especially on the right side, T2WI, FLAIR, DWI are all high signal, ADC image is low signal 

    Epilepsy-mediated brain imaging changes 

    Epilepsy-mediatedbrain imaging changes 

    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 hyperintensity on T2WI, and about half show hyperintensity on DWI.
    Commonly involved sites include cortex/subcortical area, basal ganglia, white matter, corpus callosum, and cerebellum, but there are no other specific clinical manifestations, as shown in Figure 2


    .


    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 hyperintensity on T2WI, and about half show hyperintensity on DWI.
    Commonly involved sites include cortex/subcortical area, basal ganglia, white matter, corpus callosum, and cerebellum, but there are no other specific clinical manifestations, as shown in Figure 2



    Figure 2 Two head MR findings in a 42-year-old woman with prolonged subclinical status epilepticus


    Creutzfeldt-  Jakob disease 

    Creutzfeldt–Jakob disease (CJD) is a class of infectious and progressive neurodegenerative diseases caused by prion virus, mainly manifesting as progressive dementia, mental disorders, and myoclonus


    .


    Creutzfeldt–Jakob disease (CJD) is a class of infectious and progressive neurodegenerative diseases caused by prion virus, mainly manifesting as progressive dementia, mental disorders, and myoclonus


    Figure 3 Lace sign (ribbon sign), sporadic CJD patients, A and B are DWI, C is ADC map, D is FLAIR
    .
    Asymmetric DWI hyperintensity (arrow) in the bilateral cortex of the patient can be seen, DWI hyperintensity in the basal ganglia (triangular arrow), low signal on ADC map of the lesion, and high signal on FLAIR 

    Figure 3 Lace sign (ribbon sign), sporadic CJD patients, A and B are DWI, C is ADC map, D is FLAIR
    .
    Asymmetric DWI hyperintensity (arrow) in the bilateral cortex of the patient can be seen, DWI hyperintensity in the basal ganglia (triangular arrow), low signal on ADC map of the lesion, and high signal on FLAIR 

    Mitochondrial encephalomyopathy with hyperlactatemia and stroke-like episodes 

    Mitochondrial encephalomyopathy with hyperlactatemia and stroke-like episodes  Mitochondrial encephalomyopathy with hyperlactatemia and stroke-like episodes 

    Mitochondrial encephalomyopathy is a complex group of diseases involving multiple systems with extensive biochemical and genetic defects


    .


    Mitochondrial encephalomyopathy is a complex group of diseases involving multiple systems with extensive biochemical and genetic defects
    .


    Figure 4 MELAS patient, A is DWI, high signal can be seen on cortical/subcortical DWI, B is ADC map, low signal can be seen in the lesion, C is FLAIR, high signal can be seen in the lesion, D is the patient's chronic phase FLAIR, and the lesion almost disappeared , atrophy of the affected part of the brain 

    Diffuse cerebral ischemia-hypoxic changes 

    Diffuse cerebral ischemia - hypoxia changes  Diffuse cerebral ischemia - hypoxia changes 

    DWI and ADC maps are the best sequences showing early ischemia-hypoxic brain tissue signal changes (better than T2WI and FLAIR) , and there are obvious DWI high signal and ADC low signal changes in the early stage, which most often occur in the cortex of the watershed area.
    / Subcortical, basal ganglia are also frequently involved
    .
    A clear history of diffuse cerebral ischemia and hypoxia, such as cardiac arrest, is not difficult to diagnose
    .
    Figure 5 shows a typical image performance
    .

    DWI and ADC maps are the best sequences showing early ischemia-hypoxic brain tissue signal changes (better than T2WI and FLAIR) , and there are obvious DWI high signal and ADC low signal changes in the early stage, which most often occur in the cortex of the watershed area.
    / Subcortical, basal ganglia are also frequently involved
    .
    A clear history of diffuse cerebral ischemia and hypoxia, such as cardiac arrest, is not difficult to diagnose
    .
    Figure 5 shows a typical image performance
    .

    Figure 5 In patients with cardiac arrest, diffuse cerebral ischemia-hypoxia changes, A~D is DWI, E~H is FLAIR, diffuse bilateral cortical hyperintensity can be seen 

    Figure 5 In patients with cardiac arrest, diffuse cerebral ischemia-hypoxia changes, A~D is DWI, E~H is FLAIR, diffuse bilateral cortical hyperintensity can be seen 

    other 

    other  _ 

    There are also some other diseases that can make cortical/subcortical DWI hyperintensity changes, such as posterior reversible encephalopathy syndrome (PRES) , hemiplegic migraine, moyamoya disease and so on
    .
     

    There are also some other diseases that can make cortical/subcortical DWI hyperintensity changes, such as posterior reversible encephalopathy syndrome (PRES) , hemiplegic migraine, moyamoya disease and so on
    .
     
    1. Some patients with sporadic or familial hemiplegic migraine may find cortical T2WI/FLAIR hyperintensity on MRI scans, while DWI may show isointense, hyperintensity, and hypointensity
      .
      These signal changes are transient
      .

    2. The typical lesions of PRES are bilateral lesions involving the posterior parietal and occipital lobes, often involving the middle and posterior arterial watersheds
      .
      However, the cortex is also one of its frequently involved sites
      .
      PRES generally does not show hyperintensity on DWI, but when it comes to local infarction, DWI can show hyperintensity, which often indicates a poor prognosis
      .

  • Some patients with sporadic or familial hemiplegic migraine may find cortical T2WI/FLAIR hyperintensity on MRI scans, while DWI may show isointense, hyperintensity, and hypointensity
    .
    These signal changes are transient
    .

  • Some patients with sporadic or familial hemiplegic migraine may find cortical T2WI/FLAIR hyperintensity on MRI scans, while DWI may show isointense, hyperintensity, and hypointensity
    .
    These signal changes are transient
    .

    Some patients with sporadic or familial hemiplegic migraine may find cortical T2WI/FLAIR hyperintensity on MRI scans, while DWI may show isointense, hyperintensity, and hypointensity
    .
    These signal changes are transient
    .
  • The typical lesions of PRES are bilateral lesions involving the posterior parietal and occipital lobes, often involving the middle and posterior arterial watersheds
    .
    However, the cortex is also one of its frequently involved sites
    .
    PRES generally does not show hyperintensity on DWI, but when it comes to local infarction, DWI can show hyperintensity, which often indicates a poor prognosis
    .

  • The typical lesions of PRES are bilateral lesions involving the posterior parietal and occipital lobes, often involving the middle and posterior arterial watersheds
    .
    However, the cortex is also one of its frequently involved sites
    .
    PRES generally does not show hyperintensity on DWI, but when it comes to local infarction, DWI can show hyperintensity, which often indicates a poor prognosis
    .

    The typical lesions of PRES are bilateral lesions involving the posterior parietal and occipital lobes, often involving the middle and posterior arterial watersheds
    .
    However, the cortex is also one of its frequently involved sites
    .
    PRES generally does not show hyperintensity on DWI, but when it comes to local infarction, DWI can show hyperintensity, which often indicates a poor prognosis
    .

    In retrospect, the cortical/subcortical diseases are mainly as described above, many of which require a clear medical history of the patient, such as epilepsy/status epilepticus, cerebral ischemia-hypoxia, history of migraine, etc.
    , while several others It is not difficult to identify through other clinical data.
    When necessary, MELAS can perform magnetic resonance spectroscopy, genetic examination, etc.
    , while CJD needs to improve EEG and cerebrospinal fluid 14-3-3 protein examination
    .

    In retrospect, the cortical/subcortical diseases are mainly as described above, many of which require a clear medical history of the patient, such as epilepsy/status epilepticus, cerebral ischemia-hypoxia, history of migraine, etc.
    , while several others It is not difficult to identify through other clinical data.
    When necessary, MELAS can perform magnetic resonance spectroscopy, genetic examination, etc.
    , while CJD needs to improve EEG and cerebrospinal fluid 14-3-3 protein examination
    .

    Introduction to the principle of DWI

    Introduction to DWI Principle Introduction to DWI Principle

    In order to understand the concept of DWI, it is necessary to understand both free and restricted diffusion within the cellular microenvironment
    .
    In 1827, Brown observed the pollen particles suspended in water with a microscope and found that the pollen particles kept making random movements in the water
    .
    The constant random motion of free water molecules is called Brownian motion
    .
    In contrast, the movement of water molecules within the cellular microenvironment is hindered by interactions between cellular compartments
    .

    In order to understand the concept of DWI, it is necessary to understand both free and restricted diffusion within the cellular microenvironment
    .
    In 1827, Brown observed the pollen particles suspended in water with a microscope and found that the pollen particles kept making random movements in the water
    .
    The constant random motion of free water molecules is called Brownian motion
    .
    In contrast, the movement of water molecules within the cellular microenvironment is hindered by interactions between cellular compartments
    .

    The DWI sequence is a sequence that reflects the free dispersion of water molecules
    .
    There are two main reasons for DWI hyperintensity, one is true diffusion limitation, and its ADC value is reduced; the other is a high signal with unrestricted diffusion, whose ADC value does not decrease, mainly because of the T2 projection effect
    .
    There are three main reasons for the restricted diffusion: one is cytotoxic edema, the other is increased cell density, and the third is increased fluid viscosity
    .

    The DWI sequence is a sequence that reflects the free dispersion of water molecules
    .
    There are two main reasons for DWI hyperintensity, one is true diffusion limitation, and its ADC value is reduced; the other is a high signal with unrestricted diffusion, whose ADC value does not decrease, mainly because of the T2 projection effect
    .
    There are three main reasons for the restricted diffusion: one is cytotoxic edema, the other is increased cell density, and the third is increased fluid viscosity
    .

     

    Figure 1 Principle of diffusion limitation

    Figure 1 Principle of diffusion limitation

    The T2 projection effect is the hyperintensity of DWI due to prolongation of T2 without a decrease in ADC value
    .
    Therefore, hyperintense lesions on DWI may reflect strong T2 transmission effects rather than true reduction in diffusion (Fig.
    2)
    .
    Common diseases with high signal intensity on DWI include cerebral infarction, brain abscess, brain tumor, demyelinating disease, metabolic toxicity disease, CJD,
    etc.

    The T2 projection effect is the hyperintensity of DWI due to prolongation of T2 without a decrease in ADC value
    .
    Therefore, hyperintense lesions on DWI may reflect strong T2 transmission effects rather than true reduction in diffusion (Fig.
    2)
    .
    Common diseases with high signal intensity on DWI include cerebral infarction, brain abscess, brain tumor, demyelinating disease, metabolic toxicity disease, CJD,
    etc.

    Figure 2 T2 transmission effect (35-year-old female, multiple sclerosis)

    Figure 2 T2 transmission effect (35-year-old female, multiple sclerosis) cerebral infarction DWI sequence of cerebral infarction is the main examination method for the diagnosis of cerebral infarction
    .
    In the first few minutes of cerebral infarction, the energy metabolism of brain tissue is destroyed, Na-K+/ATPase and other ion pumps are exhausted, the ions inside and outside the cells are out of balance, and a large amount of extracellular water enters the cells, forming cytotoxic edema
    .
    The water content of the whole infarct area did not increase, but the water content inside and outside the cells changed
    .
    At this time, T2WI, T1WI and FLAIR cannot show the lesions, and only the DWI that can show the diffusion movement of water molecules can show the lesions
    .
    Figure 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 of the extracellular space, and diffusion of water molecules in the infarcted area Decrease, the ADC value becomes smaller, DWI shows a high signal, and the ADC map shows a low signal
    .
    DWI hyperintensity can be displayed as early as 30 minutes
    .
    With the prolongation of time, the DWI signal gradually decreased
    .
    Brain abscess Brain abscess I put two ring-enhanced images first.
    You can guess which is a brain abscess and which is a brain tumor
    .
    Figure 4 DWI is a good method to differentiate brain abscesses from high-grade gliomas and metastases
    .
    For the two cases in the above figure, in fact, if a DWI sequence is added, it is easy to distinguish
    .
    The patient in the left picture has obvious high signal on DWI and low signal on ADC map, which is a brain abscess; the patient on the right has low signal on DWI and high signal on ADC map, which is a brain tumor
    .
    Figure 5 Contrast of annular enhancement (brain abscess vs glioblastoma)Brain abscesses are mainly hematogenous infections , most common in the frontal and parietal lobes, and less than 15% in the posterior fossa, mostly located at the gray-white matter junction
    .
    Usually single, multiple rare infections (immunosuppressed state is more common)
    .
    The pus shows long T1 and long T2, FLAIR low signal, DWI high signal, ADC low signal; the pus wall contains fibrous components, T1 is iso/slightly high signal, T2 is iso/slightly low signal, uniform annular enhancement (smooth ).
    , deep thin, superficial thick) ; there may be sub-focus (satellite lesions) , the formation of small abscesses after rupture
    .
    The smoothness of the abscess wall: purulent > tuberculous > fungal
    .
    DWI uniformity: purulent and tuberculous are more uniform, and fungal is less uniform .
    Figure 6 Brain abscess (diffusion limited) Clinically, brain abscesses are sometimes difficult to differentiate from metastatic tumors and other diseases.
    Please refer to Table 2 for the identification points .
    Brain tumor DWI signal of brain tumor mainly depends on 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 nucleocytoplasmic ratio, and increased extracellular matrix (Figure 9) .
    High-grade glioma (including anaplastic glioma, anaplastic oligodendroglioma, glioblastoma, etc.
    ) , lymphoma , metastases, medulloblastoma, central neurocytoma, primitive neuroectoderm Brain tumors such as tumor PNET usually show high signal on DWI and low ADC value .
     The relative ADC value of lymphoma : lymphoma<high-grade glioma<metastasis
    .
    For gliomas, low-grade gliomas have a slightly lower cell density and are iso- or slightly hyperintense on DWI, while high-grade gliomas have higher cell density, high DWI, and lower ADC values
    .
    This is not absolute, because DWI hyperintensity also includes T2 signal.
    Therefore, some tumors contain both ADC hypointensity (diffusion-limited part) and iso/ hyperintensity (part of T2 projection effect) in some tumors
    .
    Typical imaging manifestations of different brain tumors Typical imaging manifestations of different brain tumorsFig.
    7 Pilocytic astrocytoma (DWI isointense) Fig.
    8 Low-grade oligodendroglioma (high DWI, high ADC) Fig.
    9 Glial Blastoma (high DWI, low ADC) Figure 10   Brain metastases from lung cancer (high signal on DWI, low ADC) Lung cancerFigure 11 Lymphoma (dense tumor cells, high DWI, low ADC) Figure 12 Medulloblastoma (high DWI, low ADC ) Low) Figure 13 Central neurocytoma (dense tumor cells, high DWI, low ADC) Figure 14 Primitive neuroectodermal tumor PNET (high DWI, low ADC) Leave a message here
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