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Magnetic resonance imaging changes related to acute seizure activity

Magnetic resonance imaging changes related to acute seizure activity
Andrew J Cole, MD, FRCP(C)
Section Editors:
Steven C Schachter, MD
Glenn A Tung, MD, FACR
Deputy Editor:
John F Dashe, MD, PhD
Literature review current through: Dec 2022. | This topic last updated: Mar 02, 2021.

INTRODUCTION — The recognition of peri-ictal changes on neuroimaging studies predates magnetic resonance imaging (MRI), with reports of computed tomography (CT) abnormalities in occasional patients presenting with seizures. These findings of effacement of gyral markings and patchy contrast enhancement appeared to colocalize with the source of the ictal activity [1]. As MRI has become standard in the evaluation of patients with seizures and epilepsy, a growing range of peri-ictal imaging findings have been described. Knowledge of these findings is important because [2-4]:

These findings may be confused with other focal pathology such as brain tumor, stroke, or encephalitis, leading to inappropriate treatments or investigations.

These findings may be helpful in surgical planning.

These findings may help elucidate pathophysiology of epileptic seizures.

This topic discusses ictal and early postictal findings on MRI; we will refer to these findings together as peri-ictal. The use of MRI and other neuroimaging techniques in the diagnosis of seizures and epilepsy and in presurgical evaluation of epilepsy patients is discussed separately. (See "Surgical treatment of epilepsy in adults" and "Evaluation and management of the first seizure in adults".)

LOCAL PERI-ICTAL MRI FINDINGS — Peri-ictal imaging changes may occur in the region of the epileptic discharge (local) or in distant structures (remote). These findings are summarized in the table (table 1).

Local anatomic abnormalities — Local anatomic abnormalities are those confined to the region of epileptic discharge, and include [3-22]:

Local swelling – effacement of sulci and gyral markings (image 1)

Increased T2 signal intensity (image 1)

Restricted diffusion – bright signal on diffusion weighted imaging (DWI), dark signal on apparent diffusion coefficient (ADC) maps

Focal parenchymal and/or leptomeningeal contrast enhancement

Computed tomography (CT) is less sensitive for these changes compared with magnetic resonance imaging (MRI), but it can also show decreased attenuation, effacement of sulci, loss of gray/white differentiation, and contrast enhancement [3,23].

It is not known why local acute peri-ictal changes on MRI occur in some but not all patients. While most reported cases with these findings are associated with status epilepticus or seizure clusters, these findings have also been described after single seizures [6-9,11,24]. In one series of 69 patients with status epilepticus, 28 percent of patients had cortical and/or thalamic diffusion restriction on MRI that was deemed related to seizure based on clinical course and follow-up imaging; predictors of peri-ictal changes included regional/unilateral epileptiform discharges, periodic lateralized epileptiform discharges (PLEDs), and repetitive seizure patterns [25]. Smaller series have documented DWI abnormalities in an even higher proportion of patients with focal status epilepticus (40 to 100 percent) [16,26,27].

In some cases, MRI changes are first apparent days or weeks after the start of focal status, suggesting that there may be a threshold of seizure duration and/or severity below which changes will not occur [5,16,28]. Other patient-specific variables may play a role, such as the seizure type and location, the duration and severity of ictal discharge, pharmacologic interventions, and the patient's age, comorbid conditions, and cardiovascular or metabolic reserve. In one small series, restricted diffusion on MRI was more likely with a neocortical rather than a medial temporal focus [24].

Peri-ictal MRI findings usually resolve on follow-up imaging; however, residual T2 signal abnormalities can persist for several months, sometimes indefinitely [16-18]. Focal atrophy in the region of T2 and DWI signal changes is also often reported on follow-up imaging, but these studies are usually compared with the peri-ictal study, not a preictal baseline [3-5,7,29]. This evolution of findings has also been documented in animal studies of induced epileptic seizures and suggests that these MRI findings are the result, not the cause, of the seizure [30]. Case reports of these findings resolving with treatment and then reappearing with recurrent seizure activity also support this association [5,15].

An exceptional case report documents a patient with multifocal epilepsy related to mitochondrial disease [2]. Migratory T2 and DWI lesions appeared on serial MRI scans (image 2). These lesions corresponded to regions of focal hypermetabolism on positron emission tomography (PET) (image 3), as well as to areas of maximal electroencephalogram (EEG) abnormality. This case provides further evidence that these MRI lesions are the consequence of the epileptic activity and not its cause.

DWI images may be misleading. For example, in patients presenting with paraneoplastic or autoimmune limbic encephalitis associated with antibodies against the leucine rich glioma inactivated 1 (LGI1) protein, the N-methyl-D-aspartate (NMDA) receptor, or the gamma-aminobutyric acid B (GABA-B) receptor, DWI imaging frequently shows increased signal in the limbic structures, but ADC maps can show normal diffusion coefficients or possibly "pseudonormalization" caused by T2 shine-through [31]. The absence of true diffusion restriction should raise the question of limbic encephalitis in patients presenting with recurrent seizures, behavioral changes, and increased T2 signal in limbic structures not accompanied by focal atrophy. (See "Paraneoplastic and autoimmune encephalitis".)

Abnormalities of blood flow and perfusion — Perfusion-weighted MRI may show initial hyperperfusion in the area of ictal activity with subsequent relative hypoperfusion [5,16,32]. This temporal evolution is similar to that seen in single-photon emission computed tomography (SPECT) studies that typically show focal ictal hyperperfusion with surrounding hypoperfusion, followed by postictal hypoperfusion [33-36]. Postictal hypoperfusion on MRI can be confused with acute stroke. (See 'Impact on clinical management' below.)

Magnetic resonance angiography (MRA) in patients with status epilepticus may demonstrate a reversible prominence of arterial branches in the region of the seizure focus, with corresponding increased flow-related enhancement (figure 1) [3,5,18]. This finding corresponds with the observation of arterialization of venous blood reported by surgeons examining the cortex during provoked or spontaneous epileptic seizures (figure 1) [5,37]. SPECT studies may not demonstrate corresponding ictal hyperperfusion; thus, some portion of the local increased blood flow observed on MRA may represent arteriovenous shunting.


Diaschisis — Diaschisis is a phenomenon of functional loss in an area of the brain that is anatomically remote from the primary lesion, but neuronally connected to it. This is most often described in the setting of stroke, but can also occur with a variety of cerebral pathologies including migraine, tumor, and encephalitis [38,39]. Crossed cerebellar diaschisis, in particular, is associated with lesions in the contralateral hemisphere. In acute injury, magnetic resonance imaging (MRI) evidence of diaschisis includes restricted diffusion and increased T2 signal. These findings typically normalize over time, although, with chronic injury, volume loss in these areas may occur.

Similar MRI findings have also been described in association with acute seizure activity. Restricted diffusion and increased T2 signal in the ipsilateral diencephalon and contralateral cerebellum have been prominent findings in a number of case reports of patients in both generalized and focal status epilepticus (image 4 and image 5) [3,5,12,13,16,18,21,40-42]. These lesions usually resolved over days to weeks with control of seizures, but may presage the appearance of local atrophy of the affected structures [13,21,39,41,43]. The pathophysiology of these lesions is unknown, but presumably results from the recruitment and driving of connected thalamic and cerebellar circuits by the epileptic activity.

Lesions of the splenium of the corpus callosum — Transient lesions of the splenium of the corpus callosum have been described in patients with epilepsy [44-52]. These lesions are typically ovoid and well-circumscribed regions of increased T2 signal with restricted diffusion and resolve on follow-up imaging several weeks later (image 6) [44,48]. In most cases, this finding appears to be clinically silent, although we have noted this finding in several patients who also had psychiatric disturbances [5].

Neither the mechanism nor the precise nature of the white matter change is understood [52]. Most cases are described in patients with clusters of seizures who have been rapidly withdrawn off antiseizure medications as part of presurgical video-electroencephalography (EEG) monitoring [44-46,48-50]. Although abrupt drug withdrawal might underlie this phenomenon, this theory is based on the assumption that the splenium lesion represents vasogenic edema [46]. Our finding that the lesion demonstrates a decreased apparent diffusion coefficient (ADC) is inconsistent with that hypothesis and suggests instead that the lesion is related to ictal activity per se [44]. Microvacuolization of the myelin is one pathologic substrate that could account for the increased T2 signal, the decreased ADC, and the reversibility of lesions of the splenium. In one report, splenium lesions were associated with antiseizure medication toxicity in the absence of seizure activity, but the two cases in this report appear to be exceptional in this regard as such lesions are rarely seen in large numbers of patients who undergo MRI while on anticonvulsants [47].

Posterior reversible encephalopathy syndrome — Reversible, symmetrical, white-matter edema in the posterior cerebral hemispheres in large part defines the posterior reversible encephalopathy syndrome (PRES, also known as reversible posterior leukoencephalopathy syndrome), of which seizures are a hallmark clinical feature. PRES usually occurs in association with hypertensive encephalopathy, eclampsia, and the use of cytotoxic and immunosuppressant drugs [53,54]. However, some patients with seizures and radiologic features of PRES have none of these conditions, suggesting that seizures may be the cause or contribute to the occurrence of this MRI finding. It is usually difficult to exclude moderate elevations in systemic blood pressure with respect to the patient's baseline as a cause [55]. Moreover, the high, rather than low, ADC values that are typically seen on diffusion weighted imaging (DWI) in PRES make it at odds with other ictal MRI abnormalities [54]. (See "Reversible posterior leukoencephalopathy syndrome".)

PATHOPHYSIOLOGY — The pathophysiologic basis of local peri-ictal imaging findings appears to be related to increased neuronal activity and its associated metabolic and vascular responses. The pathophysiologic basis of lesions that occur remote from the site of ictal activity is not understood.

Whereas increased T2 signal suggests edema or gliosis, restricted diffusion is usually associated with metabolic dysfunction or energy deficiency. This phenomenon is best described in acute ischemic stroke. In this setting, restricted diffusion suggests the presence of cytotoxic edema and permanent injury. However, in the peri-ictal setting, the fact that these lesions are often reversible indicates that cell death is not an inevitable sequelae [56]. Another difference is that in ongoing status epilepticus, diffusion weighted imaging (DWI) and T2 signal changes appear to occur roughly synchronously, whereas in acute ischemia, restricted diffusion often precedes any abnormality of T2 signal. This suggests a difference in the pathophysiology of restricted diffusion in seizures and stroke; in ischemia there is early energy failure; in ongoing status, activity-induced injury with cytotoxic edema may precede overt energy deficiency. (See "Neuroimaging of acute stroke".)

It is hypothesized that prolonged ictal activity increases glucose utilization that is not adequately matched by enhanced blood flow [3,16,19]. A depletion of cellular energy reserves causes sodium-potassium adenosine triphosphatase (ATP) pump failure. This, along with the excitotoxic effects of ictal glutamate release, may trigger N-methyl-D-aspartate (NMDA) receptor-mediated calcium and water influx into the cell. A reduction in extracellular fluid causes restricted diffusion on magnetic resonance imaging (MRI) [19].

Only limited pathologic correlation for these MRI findings is available. Animal studies have shown swelling of dendrites and astrocytes [9]. In cases in which a biopsy of the affected lesion was undertaken, findings have included gliosis and cellular edema with little to no other evidence of inflammation [5,7,10]. Evidence of neuronal death is seen in some cases.

IMPACT ON CLINICAL MANAGEMENT — Local and remote peri-ictal imaging findings must be interpreted with caution. It is important to recognize that these changes can occur as the consequence of seizure activity per se and therefore may not be helpful in establishing the cause of the seizures.

In some cases, acute findings may mimic tumor, stroke, or encephalitis and if misinterpreted, would lead to inappropriate diagnostic or therapeutic interventions [3,7,57]. Because peri-ictal imaging changes evolve over time, serial imaging studies can establish the nature of these findings as peri-ictal and not related to another process (image 7).

In the setting of potential acute ischemic stroke, when treatment decisions are time-limited, the use of magnetic resonance imaging (MRI) or computed tomography (CT) perfusion studies can be helpful. The combination of hyperperfusion with increased T2 signal and restricted diffusion is uncharacteristic of ischemia [16,39,58]. If there is hypoperfusion, absence of focal or lateralized reduction of mean transit time on either the MRI or CT perfusion study suggests a postictal state rather than ischemia [58,59]. Areas of signal abnormality that do not respect vascular territories are another clue to an ictal rather than vascular origin [3]. An angiographic study may be required to detect or exclude a vascular occlusion potentially amenable to thrombolysis. (See "Neuroimaging of acute stroke".)

The variability in the occurrence of these findings is such that acute MRI changes have little utility in the routine diagnostic evaluation of patients with seizures [16]. Because some acute MRI changes are remote from the site of maximal ictal activity, it is important to evaluate imaging abnormalities in conjunction with clinical and electrographic data; however, when these findings are convergent, it may support a plan for early surgical intervention and help in the process of surgical planning [10].

In exceptional patients, MRI may be useful to assess the efficacy of antiseizure treatment. We and others have observed that in focal status epilepticus, anesthesia sufficient to suppress seizure activity also results in reversal of imaging abnormalities [5,32]; this finding might be exploited in settings in which electroencephalogram (EEG) activity is difficult to monitor.

SUMMARY — Magnetic resonance imaging (MRI) studies performed during or immediately after epileptic seizure can show structural abnormalities that are understood to represent the effect of the seizures rather than the underlying cause. These findings are summarized in the table (table 1).

The most common acute peri-ictal MRI changes occur at the site of seizure focus and include local swelling, T2 signal hyperintensity, restricted diffusion, and contrast enhancement. (See 'Local anatomic abnormalities' above.)

Perfusion MRI and magnetic resonance angiography can also show evidence of seizure-related blood flow changes, including increased prominence of blood vessels and ictal hyperperfusion in the region of epileptic discharge. Hypoperfusion characterizes the immediate postictal state. (See 'Abnormalities of blood flow and perfusion' above.)

MRI changes that occur in brain areas remote from the seizure focus include signal changes in the ipsilateral diencephalon and contralateral cerebellum. (See 'Remote peri-ictal MRI findings' above.)

The pathophysiology of these changes is not well understood, but likely reflects the consequences of increased neuronal activity and its associated metabolic and vascular responses. (See 'Pathophysiology' above.)

The most important clinical caveat regarding acute peri-ictal MRI findings is to recognize that such findings may be the consequence, rather than the cause, of the seizures so as to avoid inappropriate diagnostic and therapeutic interventions. Follow-up imaging is generally sufficient for this distinction. However, in the setting of acute ischemic stroke adding perfusion studies (computed tomography [CT] or MRI) and/or angiography can be valuable in treatment decisions. (See 'Impact on clinical management' above.)

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