Abnormal MRI after a seizure, what do you think?

For patients with epileptic seizures in clinical work, we can occasionally find abnormal signals on MRI of his head
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Identifying whether these imaging findings are the primary focus of the disease or post-ictal changes is important for neurologists, especially when dealing with emergency patients
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This article mainly introduces the identification and analysis of MRI changes in patients with epileptic seizures
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Author: Tsai This article is published with the authorization of the author, and please do not reprint without authorization
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What is the brain doing during/after a seizure? We know that seizures are clinical manifestations caused by abnormal, excessive, and hypersynchronous firing of cortical neuron clusters
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In short, it is a series of symptoms caused by excessive excitation and abnormal discharge of neurons
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Understanding the pathophysiological state of neurons during epileptic seizures is the first step in solving the case
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To help understand the process of seizures, we simply interpret them in a "who-how-why" format
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 ① First, "who" is the initiating unit of discharge, mainly refers to the cortex, which is divided into projection/primary neurons (such as pyramidal neurons) and interneurons (such as basket cells)
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The former refers to cells that "project" or send information to neurons located in distant regions of the brain; the latter are often thought of as local circuit cells that influence the activity of nearby neurons
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Most often, projection neurons form excitatory synapses on postsynaptic neurons, while interneurons form inhibitory synapses on chief cells or other inhibitory neurons
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Repetitive inhibition occurs when projection neurons synapse on inhibitory neurons, which in turn synapse on principal cells to achieve a negative feedback loop
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In addition, some interneurons may have extensive axonal projections that can provide strong synchronization or pacemaker activity to large numbers of neurons
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 ② The understanding of "how" needs to start from the action potential
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Increased excitatory synaptic neurotransmission, decreased inhibitory neurotransmission, changes in voltage-gated ion channels, or changes in intracellular or extracellular ion concentrations favor membrane depolarization, causing neuronal hyperexcitability
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In this process, the release of excitatory (mainly glutamate) and inhibitory neurotransmitters (mainly GABA) at synaptic terminals is critical (Table 1)
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Table 1 Abbreviations for glutamate receptors and GABA receptors: AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor; GABAR=GABA=γ-aminobutyric acid receptor; GluR=glutamate receptor; NMDAR=N-methyl d-aspartate receptor
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 ③ After understanding the basic structural framework, we will analyze the "why" problem next
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Why do neuronal excitability change? Triggered by what? What is the situation that causes epilepsy? Neuronal activity is complex and involves the regulation of electrical activation levels in one or more cellular regions by a variety of factors, both intrinsic and extrinsic to the neuron
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Among them, intrinsic factors mainly refer to factors inside neurons, while extrinsic factors refer to the cellular environment, including other cells (such as neighboring neurons, glial and vascular endothelial cells) and the extracellular space (Table 2)
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In addition, there are complex connections between neurons, with additional control over neuronal excitability
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Table 2 Summary of neuronal intrinsic and extrinsic factors Seizures include two concurrent events: 1) high-frequency bursts of action potentials; 2) hypersynchrony of neuronal clusters
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Epilepsy propagation occurs when there is sufficient activation to recruit peripheral neurons, causing a loss of peripheral inhibition and the spread of epileptic activity to adjacent areas via local cortical connections and to more distant regions via long associative pathways such as the corpus callosum area
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In contrast, intact hyperpolarized and inhibitory neurons produce peripheral areas of inhibition that prevent the spread of burst activity
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 The specific mechanism of epileptic seizures caused by abnormal central nervous system is still unclear, but it is related to the pathological process caused by the disturbance of the balance of excitation and inhibition
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Namely, changes in extracellular ion homeostasis, altered energy metabolism, receptor function, or altered transmitter uptake processes lead to synchronous bursts of cortical neurons leading to seizures, and the location and function of abnormal neuronal networks during this process can lead to different Epilepsy phenotype
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Among them, some forms of epilepsy can be caused by specific events, such as about 50% of patients with severe head injury can progress to epilepsy, but can be clinically asymptomatic in the preceding months to years, suggesting the existence of "after the initial injury" "Silent period"—a process during which the neural network gradually transitions over time, with delayed necrosis of inhibitory interneurons, or sprouting of axonal collaterals leading to enhanced circuits
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 Do seizures cause abnormal imaging changes? You can probably guess the answer to this question
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As mentioned above, epileptic seizures involve the imbalance of neuronal excitation and inhibition, and during this process, neurons and glial cells may also show corresponding ischemia and hypoxia manifestations, which can lead to imaging abnormalities in severe cases
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 According to the area of ​​epileptic discharge (local) and the distant area, the imaging abnormalities can be divided into two categories (Table 3)
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 Table 3 Abnormal imaging changes of local and distant sites caused by epileptic seizures Abnormal signals on MRI of the right thalamus and hippocampus in patients with status epilepticus T2 hyperintensity involving the hippocampus and extending to the right thalamus with limited diffusion and no enhancement of the lesion may be associated with status epilepticus (Katramados AM, et al.
Epilepsia, 2009, 50(2): 265-275.
)
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 Are MRI abnormalities cause or effect? In the clinical process, imaging abnormalities that appear after a seizure must be cautious, and it is necessary to identify whether it is the result of the epileptic activity itself or the cause of the seizure
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In the identification of etiology, acute manifestations may resemble tumors, stroke, or encephalitis, and further identification is required
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In addition to the associated imaging abnormalities described above, peri-ictal imaging changes evolve over time, and serial imaging studies can characterize these findings as peri-ictal and independent of other processes
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For the identification of acute ischemic stroke, MRI and CTP can be further identified to help early diagnosis and treatment - hyperperfusion + T2 hyperintensity + diffusion restriction are the characteristics of stroke; when there is hypoperfusion, MRI or CT perfusion study There was no focal or lateral reduction in mean transit time, suggesting a postictal state rather than ischemia
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In addition, an area of ​​signal abnormality regardless of the vascular region is another clue to the episode rather than the vascular origin, and angiography is helpful for further identification
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In addition, combining clinical and EEG facilitates further identification
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 SUMMARY Seizures (especially status quo) can lead to abnormal intracranial imaging, partly cause, partly effect, and easily confused with other diseases
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Therefore, attention should be paid to the clinical diagnosis and treatment process, and MRI and other technologies can help to further identify
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