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| LETTER TO EDITOR |
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| Year : 2022 | Volume
: 39
| Issue : 4 | Page : 213-215 |
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The value of arterial spin labeling magnetic resonance imaging in the periictal period: A case with continuous lateralized periodic discharges
Nese Dericioglu1, Rahsan Göçmen2
1 Department of Neurology, Faculty of Medicine, Hacettepe University, Sihhiye, Ankara, Türkey
2 Department of Radiology, Faculty of Medicine, Hacettepe University, Sihhiye, Ankara, Türkey
| Date of Submission | 10-May-2022 |
| Date of Decision | 11-Aug-2022 |
| Date of Acceptance | 23-Aug-2022 |
| Date of Web Publication | 19-Dec-2022 |
Correspondence Address:
Nese Dericioglu
Department of Neurology, Faculty of Medicine, Hacettepe University, Sihhiye 06100, Ankara
Türkey
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/nsn.nsn_85_22
How to cite this article:
Dericioglu N, Göçmen R. The value of arterial spin labeling magnetic resonance imaging in the periictal period: A case with continuous lateralized periodic discharges. Neurol Sci Neurophysiol 2022;39:213-5 |
How to cite this URL:
Dericioglu N, Göçmen R. The value of arterial spin labeling magnetic resonance imaging in the periictal period: A case with continuous lateralized periodic discharges. Neurol Sci Neurophysiol [serial online] 2022 [cited 2023 Jun 4];39:213-5. Available from: http://www.nsnjournal.org/text.asp?2022/39/4/213/364424 |
Dear Editor,
There has been an ongoing debate about the ictal/interictal nature of lateralized periodic discharges (LPD), and they have often been accepted to lie in the interictal/ictal continuum.[1] When accompanied by focal clonic/myoclonic movements as is evident in epilepsia partialis continua, LPDs represent an ictal phenomenon.[2] The significance of LPDs is harder to determine when there are no motor signs. In such circumstances, it is reasonable to conclude that some LPDs in some patients can be ictal, whereas others are interictal findings. This dichotomy, on the other hand, has implications for treatment strategies. Several previous case reports have utilized single-photon emission computed tomography (SPECT), diffusion-weighted (DWI) and perfusion-weighted (PWI) magnetic resonance imaging (MRI), or positron emission tomography (PET) techniques to demonstrate the ictal nature of this particular electroencephalography (EEG) pattern.[3],[4],[5],[6],[7] Here, we report an elderly male subject with continuous LPDs over the left parietooccipital region, whose DWI and PWI imaging techniques suggested nonconvulsive status epilepticus (NCSE) before long-term EEG monitoring.
An 83-year-old male patient was admitted to the emergency department of our center after two generalized tonic–clonic seizures, for the first time in his life. On admission, blood biochemistry results were within normal limits. Complete blood count suggested iron deficiency anemia and leukocytosis. Structural MRI revealed multiple necrotic metastases in the infra- and supratentorial regions [Figure 1]a. Diffusion-weighted imaging and apparent diffusion coefficient suggested cytotoxic edema over the left parietooccipital cortex. The lack of cortical contrast enhancement ruled out stroke-like migraine attacks after radiation therapy syndrome [Figure 1]b and [Figure 1]c. He did not regain consciousness after the seizures. Hence, he was loaded with 3000 mg levetiracetam (LEV) and put on 2 × 1000 mg/day as a maintenance dose. An emergent EEG revealed moderate background slowing with continuous LPDs in the left occipital area [Figure 2]a. His history revealed non-small cell lung cancer, for which he received chemotherapy (CT) and radiotherapy (RT) 3 years ago. One year later, he developed difficulty with walking. After the discovery of a left cerebellar metastatic lesion, he was operated and received RT. Due to his deteriorating general status, he could not receive further CT. He became dependent on everyday living. His level of consciousness was fluctuating, and he had difficulty with swallowing. | Figure 1: Axial postcontrast T1-weighted image demonstrating two parenchymal metastases (arrows) in the left temporal and occipital lobe (a). Diffusion-weighted image reveals restricted diffusion in this region (b, arrow), and a lack of abnormal contrast enhancement is noted at the same level postcontrast image (c). Arterial spin labeling MR perfusion – cerebral blood flow maps (d-f) reveal definite hyperperfusion in the left parietooccipital cortex (d-f, long arrow), ipsilateral posterior thalamus (e, short arrow), and hippocampus (f, short arrows). Furthermore, note subtle cortical hyperperfusion in the whole left hemisphere (d, short arrows). MR: Magnetic resonance
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 | Figure 2: EEG epoch is consistent with 1 Hz lateralized periodic sharp waves over the left occipital area (a). Prolonged EEG monitoring reveals continuous lateralized periodic discharges with superimposed spikes or rhythmic waves on some complexes (b). Spike mapping shows that area with maximum negativity is in the left occipital region (c). Electrographic seizure is characterized by rhythmic sharp waves and spikes in the left parietooccipital region, lasting about 11 s (d). EEG: Electroencephalography
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The patient partly regained consciousness after antiseizure medication (ASM) loading but had difficulty with cooperation and did not return to baseline functional level. Since NCSE could not be ruled out, a PWI with arterial spin labeling (ASL) was requested which demonstrated increased blood flow in the left parietooccipital region, left thalamus, and hippocampus [Figure 1]d, [Figure 1]e, [Figure 1]f. Lacosamide 2 × 100 mg/day was added to LEV. The next day, the patient was transferred to the neurology inpatient clinic where continuous video – EEG monitoring was performed for 4.5 h. There was moderate background slowing with LPDs over the left parietooccipital region [Figure 2]b and [Figure 2]c. Spikes or rhythmic activity was superimposed on some complexes. Besides, two electrographic seizures characterized by rhythmic sharp waves, with superimposed spikes, lasting 10–12 s over the same area were recorded [Figure 2]d. Benzodiazepine injection was not performed at the onset of continuous EEG due to respiratory insufficiency. We added topiramate 2 × 25 mg/day and clonazepam 1 × 1 mg/day to existing ASMs. Due to multiple medical comorbidities, the patient was transferred to the neurosurgery intensive care unit. Several control EEG recordings revealed the presence of frequent sharp waves over the left occipital area that had lost their periodicity. On follow-up, the patient did not improve further and died 1 month later due to sepsis and multiple organ failure.
In critically ill patients, it may be hard to interpret the clinical significance of LPDs. Recently, a set of criteria including clinical, neuroimaging, and EEG has been proposed.[1] Regarding EEG, LPDs-proper are considered interictal discharges due to irritative brain lesions. LPDs-plus, on the other hand, are accepted as periictal or ictal. These are periodic discharges with superimposed fast activity, rhythmic activity, spikes/sharp waves, or discharges having a triphasic morphology.[8] In our case, the initial LPDs had a somewhat sharp character, but it was not easy to decide if they were LPD-plus or not. Although we planned a prolonged EEG monitoring, the patient could not be transferred to the neurology inpatient service. Meanwhile, we preferred to proceed with ASL imaging. Finally, clinical findings (having clinical seizures, failure to return to baseline functional level), EEG, and imaging results suggested NCSE. The detection of two electrographic seizures with continuous EEG further supported the diagnosis. In our patient, NCSE was most likely induced by metastatic brain lesions. Rarely, it has also been reported to occur after a single convulsive episode, in which case it is usually accompanied by periodic discharges. The infection could be another plausible explanation due to leukocytosis; however, it was probably a nonspecific inflammatory reaction to seizures as other parameters did not support the presence of a systemic or central nervous system infection at presentation.
Few centers are able to perform continuous EEG in critically ill patients. Therefore, investigators have searched for additional techniques that rely on alterations in brain perfusion and metabolism, such as DWI, PWI, SPECT, and PET. The last two techniques are often difficult to perform in emergency situations, whereas MRI is readily available in most centers. Previous studies with DWI and PWI have demonstrated the utility of these techniques in the periictal period.[3] Seizure-related increase in glucose and oxygen demand leads to local hyperperfusion. ASL perfusion is a type of PWI that uses magnetically labeled water in the blood as an endogenous tracer. There is no need for intravenous Gadolinium infusion. It has a sensitivity of 65%–90% for identifying the seizure focus, and is superior to DWI and traditional dynamic susceptibility contrast perfusion.[4],[9] Few studies have investigated the utility of ASL imaging in status epilepticus, with several patients having LPDs.[4],[5],[6],[9] Besides cortical hyperperfusion, involvement of the ipsilateral thalamus and hippocampus was reported in rare cases, like our patient.[3],[4],[6] Involvement of the thalamus has been thought to occur due to reciprocal connections between the thalamus and the temporoparietal cortex.[4] Ohtomo et al. reported that thalamic hyperperfusion with ASL correlated with NCSE, periodic discharges, and rhythmic delta activity.[6] In status epilepticus, the hippocampus was affected in 65%–80% of the patients on DWI.[3],[10]
In conclusion, we suggest that in cases where NCSE is suspected but continuous EEG monitoring cannot be performed, or it is hard to decide if LPDs are ictal and need more aggressive treatment, neurologists can ask for DWI and PWI preferably with ASL. It should also be kept in mind that these neuroimaging modalities are nonspecific markers for seizures.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
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