CLINICAL AND RESEARCH REPORTS

Levetiracetam Effect on Adult-Onset Temporal Lobe Epilepsy With Positive Voltage-Gated Potassium Channel Antibody Wei Wang, M.D., Hong-Bo Zheng, M.D., Jing Xiao, M.Med., Lei Chen, M.D., Dong Zhou, M.D.

Temporal lobe epilepsy is considered to be the most frequent of all epileptic syndromes. Recently, several retrospective studies suggest that limbic encephalitis (LE) may be a cause for adult onset unexplained seizure disorders in patients. This report describes two cases of adult onset epilepsy with voltage-gated potassium channel antibodies (VGKC-abs)-associated LE that responded well to levetiracetam (LEV). As demonstrated by these two cases and reviewing previous reports, we propose that the therapeutic regimen for VGKC-abs associated seizures still needs to be determined and LEV may be effective in treating this kind of disorders. J Neuropsychiatry Clin Neurosci 2015; 27:e100–e106; doi: 10.1176/appi.neuropsych.13070158

Temporal lobe epilepsy (TLE) is considered to be the most frequent of all epileptic syndromes. Previous researches suggested that the majority of TLEs start before the age of 20.1 Several recently retrospective studies suggest that limbic encephalitis (LE) may be a cause for the development of adult onset unexplained seizure disorders in patients.2 LE was initially identified as a paraneoplastic neurologic syndrome usually associating with intracellular onconeural antibodies, such as Hu antibodies, CV2/CRMP5 antibodies, Ma2 antibodies, and amphiphysin antibodies.3 Lately, some types of antibodies against cell membrane antigen, such as voltage-gated potassium channels antibodies (VGKC-abs), N-methyl-D-aspartate receptor (NMDAR) antibodies, and other antibodies, were found in patients who usually do not have cancer.4 Previous studies mainly focused on the features and treatments of LE. Little was known about what kind of antiepileptic drugs (AEDs) was effective in treating this kind of seizure disorders. Here, we describe two cases of adult onset TLE with VGKC-abs-associated LE in China. This is the first reported Chinese case; we propose that levetiracetam (LEV) may be a useful treatment for this kind of TLE. CASE REPORTS Case 1 A 57-year-old right-handed woman was admitted to our hospital with a 9-day history of short-term memory loss and psychiatric symptoms without fever. She suffered from recurrent episodes of fear without hallucination when few people e100

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around. Moreover, she had two episodes of generalized tonicclonic seizure (GTCS) 9 days before admission. After admission, the patient appeared to have complex partial seizure (CPS), seven to eight times per day. Physical examination showed short-term memory impairment and time disorientation. Laboratory tests demonstrated a persistent hyponatremia (1172131mmol/L) and hypochloremia (85.2–94.7mmol/L). Other routine blood tests were normal, such as chest X-ray, CSF examination, and bone marrow puncture. Electroencephalograph (EEG) showed generalized slow activity without epileptic discharges. The Mini-Mental State Examination (MMSE) score was 9/30 (illiterate). Brain MRI demonstrated bilateral increased signal in the medial part of the temporal lobe on T2-weighted and fluid-attenuation inversion recovery (FLAIR) images (Figure 1 a‒c). Positron emission tomography/computed tomography (PET/CT) showed hypermetabolism in bilateral hippocampus (Figure 1 d and e). Suspecting virus encephalitis at first, IV acyclovir (10 mg/kg for 14 days) was started, and seizures were treated with LEV (500 mg bid). Four days later, the frequency of seizure declined obviously to three to four times per day. Two weeks later, the seizure was totally under control, but the psychiatric symptoms did not improve. Fifteen days after admission, we started to give this patient IV methylprednisolone (500 mg/day for 5 days), and her symptom improved dramatically. Then, the patient continued to use AEDs (LEV 500 mg bid) after discharge. Two months later, the patient returned to our hospital for a follow-up visit. Her serum sodium level had returned to normal (139 mmol/L), and she did not have any psychiatric J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

WANG ET AL.

symptoms or episodes of seizure. MMSE score rose to 13/30 (illiterate). Furthermore, the signal of the medial temporal lobe on T2-weighted and FLAIR images had also reduced within two months (Figure 1 f‒h). Antineuronal antibodies (Hu, Yo, Ri, Ma1/2, CV2/CRMP-5, and amphiphysin) were negative. Serum VGKC-abs level and CSF VGKC-abs level before the prescription of methylprednisolone were 130.54 pmol /L and 161.14 pmol /L, respectively (cutoff value: 100 pmol/L). Antibody titers were measured with ELISA (1:5 dilution, Kingmed Diagnostics, Chengdu, China). We did not test the antibodies 2 months later because the patient refused. Case 2 A previously healthy 45-year-old woman presented with three episodes of generalized seizure evolving to status epilepticus 3 months prior to admission, each seizure lasting more than 10 minutes. She gradually developed disorientation, and psychiatric symptoms manifested as personality change, unwillingness to communicate with others, anxiety, panic, visual and auditory hallucination, persecutory delusion, and aggressive behavior. This patient had elevated TPOAb (179.20 IU/L) and TgAb (157.40 IU/L), but other hormones, such as ACTH, LH, GH, FSH, PTC were normal. She also had hyponatremia (130–133 mmol/L) and hypochloremia (95–96 mmol/L). Other laboratory and radiological examinations did not reveal any signs of infection or tumor. Her serum VGKC-abs level and CSF VGKC-abs level before the prescription of methylprednisolone were 112.35 pmol/L and 194.63 pmol/L, respectively. After that, we give the patient IV methylprednisolone (500 mg/day) and oral LEV (500 mg bid) simultaneously. However, 5 days later, the patient was automatically discharged even though her symptoms did not fully resolve. At discharge, IV methylprednisolone was stopped, and LEV was continued to be used in the same dose. When the patient returned to our hospital for a follow-up visit 2 months later, she did not have any episode of seizure and her psychiatric symptoms also improved. DISCUSSION Combining the patients’ history, laboratory tests, imaging examinations, and response to treatment, we considered these two patients to be nonparaneoplastic VGKC-abs- associated LE. This is in accordance with newly proposed diagnostic criteria for LE.5,6 VGKC-abs-associated LE constitutes approximately 30% of all autoimmune encephalitis with antibodies to cell membrane antigens.7 VGKCs are widely expressed throughout the entire nervous system and are critical in establishing the resting membrane potential and generation of neuronal action potentials, some subtypes, such as VGKC1.1, VGKC1.2, VGKC1.6, were strongly expressed in the hippocampus molecular layer.8 Recent studies suggest that these antibodies seem to target associated VGKC-complex proteins instead of Kv1 subunits. These targeted proteins include leucine-rich, glioma inactivated 1 (Lgi1), and contactin-associated protein-2 (Caspr2). In J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

FIGURE 1. Brain MRI and Positron Emission Tomography/ Computed Tomography (PET/CT) Images of the Patienta

a

[a-c] Brain MRI demonstrated bilateral hyperintense in the medial temporal lobe on T2-weighted and fluid-attenuation inversion recovery (FLAIR) images. [a] T1WI; [b] T2WI; [c] FLAIR image. [d-e]: PET/ CT showed hypermetabolism in bilateral hippocampus. [f-h] The brain MRI signal of the medial temporal lobe on T2-weighted and FLAIR images had reduced within 2 months. [f] T1WI; [g] T2WI; [h] FLAIR image.

patients with positive Lgi1-Abs, the probability of occurrence of seizure is more common than the patients with positive Caspr2-Abs.9 Because the VGKC-abs were detected using ELISA, we did not further detect the Lgi1-Abs/ Caspr2-Abs. These two cases prompted that VGKC-abs-associated LE may be an important cause for adult onset TLE. The clinical features of epilepsy in previously reported VGKC-abs-associated LE were summarized in Table 1. Case series and case reports from January 2001 to December 2013, which refer to adult onset (.18 years old) VGKC-abs-associated LE, were included in Table 1. Reviews, letters, case series, and case reports concerning other antibodies and children cases were excluded, as well as articles, which only discussed one part of LE (e.g., only MRI findings) or the clinical data are incomplete or unclear. VGKCabs-associated LE is more common in men above 40 years old. Vincent et al. reviewed 10 patients with positive VGKC-abs associated LE, and seizures were present in nine patients during the acute phase of the disease, including GTCS and/or CPS. Additional features include hallucination, agitation, and behavioral disturbance. Hyponatremia is a common symptom.10 Antibodies to VGKC may also associate with paraneoplastic neuro.psychiatryonline.org

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Germany Case series

Bien et al.12 Neurology. 2007 Zuliani et al.30 J Neurol Neurosurg Psychiatry. 2007

Graus et al.4 Neurology. 2008 Malter et al.11 Ann Neurol. 2010

USA

Thieben et al.24 Neurology. 2004

Case series

Case report

Case series

Case series

Germany Case control

Spain

Spain

UK

Vincent et al.10 Brain. 2004

Case series

UK

Pozo-Rosich et al.29 Ann Neurol. 2003

Case report

UK

Study Design

Buckley et al.28 Ann Neurol 2001

Reference

Study Location

55 (44–73)

24–44

middle age

44(24–63)

44–69

57(44–79)

47–67

47–66

Age (Years)

6:4

3:1

1:1

16:4

5:2

9:1

4:0

0:2

M:F

10/53

4/7

2/9 with paraneoplastic LE

4/7

7/7

10/10

4/15

2/2

VGKC-abs Positive Patients/ Patient Number

6/10

4/7

2/2

9/9

6/7

9/10

4/15

1/2

Epilepsy as Onset Symptom EEG

Generalized slowing, with focal sharp waves in some cases





One used VPA



slowing in the left temporal lobe or generalized slowing and epileptic activity in both temporal lobes —

Multiple AEDs All abnormal, (did not 4 had show) temporal lobe epileptic form activity — —

PHT,VPA,PB, CLB, LRZ, et al.

one with VPA; Normal the other with multiple AEDs — —

Antiepileptic Drugs Prescribed Within 6 months

Symptoms Recovery Period

7/10 bilateral mediotemporal encephalitis

9 months, all seizure free



continued

mean 17 months





— One unilateral

2/4 bilateral, 2/4 unilateral





one patient fully resolved in 4 month

, 6 months

3 months

signal reduced in 2 years

MRI recovery period

5/9 bilateral

Bilateral hyperintense — in the hippocampus or other areas of the limbic system 5/10 bilateral medial Did not show, temporal lobe high but seizure signal, 3/10 leftreduced with sided hippocampal the decline of antibodies high signal, 2/10 normal titers. Bilateral or unilateral Within 24 mesial temporal months lobe high signal

Left hippocampus abnormality

MRI Findings

TABLE 1. Summary of Clinical Features of Epilepsy in Previously Reported Voltage-Gated Potassium Channel Antibodies (VGKC-abs) Associated Limbic Encephalitisa

LEVETIRACETAM EFFECT ON ADULT-ONSET TEMPORAL LOBE EPILEPSY

J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

Shin et al.23 J South Neuroimmunol. Korea 2013

UK

57(38–73)

Germany Case control

Irani et al.33 Brain. 2013

49

Germany Case report

Case series

Case series

1:0

60.5(41–78)

68(28–92)

8:6

5:5

8:7

0:1

64(36–83) 19:10

Balint et al.32 J Neurol Sci. 2013 Frisch et al.15 Eur J Neurol. 2013.

Case series

UK

64

60(30–80) 37:20

Irani et al.20 Ann Neurol. 2011

Case report

Case control

USA

M:F

63(19–83) 44:20

Age (Years)

USA

Case control

UK

Study Design

Barajas et al.8 Epilepsia. 2010

Irani et al. Brain. 2010 Lai et al.31 Lancet Neurol. 2010

9

Reference

Study Location

TABLE 1, continued

14/14

10/10

15/31

1/1

29/29

1/1

57/57

64/64

VGKC-abs Positive Patients/ Patient Number

14/14

10/10

not certain

1/1

20/29

1/1

42/57

59/64

Epilepsy as Onset Symptom



1–3 AEDs

Average one kind of AEDs



A mean 2.6 AEDs

LEV, LTG





Antiepileptic Drugs Prescribed 40/64 had MRI medial temporal lobe high signal 43/57 had medial temporal lobe high signal 12/57 fully recovered with a follow-up of 18 months Within 24 months



Symptoms Recovery Period





MRI recovery period

neuro.psychiatryonline.org

continued

14 months multiple seizures Left hippocampus arising from and bilateral frontal the left anterior temporal lobe lobes hyperintense — diffuse slowing 10/29 bilateral, 3/29 14 showed (N=9), bilateral unilateral medial a.50% temporal lobe reduction frontotemporal slowing (N=6), high signal, in seizure temporal sharp 12/29 normal frequency waves (N=2), over the normal (N=9) first month of immunotherapy generalized Unspecific — slow activity leptomeningeal signal changes — 9/15 bilateral, 4/15 11/15 reached no MRI left-sided, 1/15 seizure-free improvement right-sided with a follow-up encephalitic mesiotemporal of 25 months MRI features Seizure — 3/10 showed 2/10 showed frequency diffuse abnormalities reduced slowing, involving medial within 6/10 was temporal lobes, 7 –144 days normal 7/10 had normal MRI — 8 had 9/14 had medial Positive epileptiform temporal lesions, response discharges, 5 of them had within a 2 had focal bilateral lesions follow-up rhythmic of 1–24 slowing wave months, 2/12 relapse

26/57 had abnormality of any kind



EEG

MRI Findings

WANG ET AL.

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AEDs: antiepileptic drugs; Caspr2: contactin-associated protein–2; CLB: clobazam; CBZ: carbamazepine; EEG: electroencephalograph; F: female; FLAIR image: fluid-attenuation inversion recovery image; HS: hippocampal sclerosis; LE: limbic encephalitis; LEV: levetiracetam; LRZ: lorazepam; LTG: lamotrigine; M: male; PB: phenobarbital; PHT: phenytoin; VGKC-abs: voltage-gated potassium channels antibodies; VPA: valproic acid; TPM: topiramate; T2WI: T2-weighted image. a

— — Meninges and cortex damage — — 1/1 1/103 1:0 67 Case series Thailand Saraya et al. BMC Neurol. 2013

Reference

34

Study Location

TABLE 1, continued

Study Design

Age (Years)

M:F

VGKC-abs Positive Patients/ Patient Number

Epilepsy as Onset Symptom

Antiepileptic Drugs Prescribed

EEG

MRI Findings

Symptoms Recovery Period

MRI recovery period

LEVETIRACETAM EFFECT ON ADULT-ONSET TEMPORAL LOBE EPILEPSY

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LE because of thymoma or small cell lung cancer, but more frequently with nonparaneoplastic LE.10 The most common abnormalities on brain MRI is increased signal in medial temporal lobe on T2-weighted and FLAIR images, either bilateral or unilateral, but it can also be normal.11, 12 In a systematic review, neuroimaging investigations revealed baseline MRI changes in 70% cases.13 A general tendency of mediotemporal signal regression is within 4–17 months (Table 1), but some patients develop into hippocampal atrophy and hippocampal sclerosis.4,12 The relevance of clinical manifestation and antibodies titers has been confirmed in many researches.14–16 With the antibodies titers declined, the clinical symptom can improve as well as the lesion on brain MRI. The antibodies titers of these two cases were relatively low, may be for the reason that the symptoms of these two cases were relatively mild and the samples were obtained at the early onset of the disease. Furthermore, the levels of VGKC antibodies in the CSF were higher in the CSF compared with serum in both cases, indicating intrathecal synthesis of antibodies, as previous reported in anti-NMDAreceptor encephalitis.17 Recently, there have been frequent descriptions of LE and refractory epilepsy (RE) secondary to antibodies to a broad variety of neuronal antigens.18,19 VGKC-complex antibodies and similar antibodies have been identified in around 10% of unselected patients with unexplained and drug-resistant epilepsy.20 For patient with RE or super RE, it is crucial to establish the underlying cause of seizures.21 Both paraneoplastic and nonparaneoplastic LE may result in RE. Recent researches suggested autoimmune encephalitis may be an essential cause of nonconvulsive status epilepticus, especially anti-NMDAR encephalitis.19 Compared with widely expressed NMDA receptors,17 antibody associated with LE that strongly affects temporal lobe is the VGKC complex antibody.22 Although the incidence of RE associated with anti-VGKC encephalitis remains to be determined, the typical medial temporal regions that anti-VGKC encephalitis affects may be a potential reason for RE.23 The main therapy for LE is immunotherapy. Corticosteroids, intravenous immune globulin (IVIg) and plasma exchange are most frequently used. Other immunosuppressive agents, such as cyclophosphamide and rituximab, can also be utilized.7,11 Although immunotherapy is widely accepted for the treatment of LE, there are many side-effects and other risks.20 Additionally, some patients respond poorly to immunotherapy and fully control of epilepsy needs a long time after immunotherapy and sometimes needs to be treated with AEDs simultaneously.17,18 Previous studies rarely focused on the treatment of seizure. Seizure in this disorder is generally difficult to control and often require treatment with multiple AEDs.24 Only few studies mentioned the AEDs they prescribed. Phenytoin (PHT), phenobarbital (PB), valproic acid (VPA), clobazam (CLB), lorazepam (LRZ), lamotrigine (LTG), carbamazepine (CBZ), topiramate (TPM) and LEV were prescribed in previous reports of patients with positive VGKC-abs (Table 1). But the relationship J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

WANG ET AL.

between the control of seizures and the prescription of AEDs didn’t point out explicitly. Thus, it is unclear which kind of AEDs is more effective for epilepsy induced by VGKC-abs associated LE. In our two cases, after using LEV, the seizure was under control, even before the administration of immunotherapy (Case # 1). In previous case reports, there are a few cases which responded well to AEDs alone.20,25 Barajas et al. also reported a case who was treated with LEV and LTG and the patient reached seizure free within 24 months.8 Until now, LEV has been proved to be safe and effective in treating acute seizure and status epilepticus.26 Swisher et al. suggested that the combination use of PHT, LEV, and pregabalin (PGB) in brain tumor patients with refractory status epilepticus is safe and highly effective.27 As demonstrated by these cases, we proposed that LEV may be a useful AEDs for seizure induced by LE. And this application did not have an obvious psychiatric adverse side effect. CONCLUSIONS In conclusion, the therapeutic regimen for VGKC-abs-associated seizure still needs to be determined. At what point to start immunotherapy, whether there is a need to administer corticosteroid along with AEDs, and what kind of AEDs should be used are still questions. These two cases indicate that LEV may be effective in treating epilepsy induced by LE. More research should be conducted to confirm this and to provide more evidence for the treatment of epilepsy induced by LE. AUTHOR AND ARTICLE INFORMATION From the Dept. of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China. Send correspondence to Drs. Lei Chen or Dong Zhou; e-mail: leilei_ [email protected] or [email protected] Drs. Wang and Zheng contributed equally to this study. Drs. Lei Chen and Dong Zhou, as the co-corresponding authors, contributed equally to this study. This study was supported by the Research Project of Chengdu Science and Technology Agency (No. 12DXYB209JH-002), the scientific research foundation of Sichuan University for outstanding young scholars (No. 2082604164246). The authors report no financial relationships with commercial interests. Received July 13, 2013; revised Dec. 22, 2013, and Feb. 16, 2014; accepted Feb. 24, 2014; published online Oct. 14, 2014.

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6. Zuliani L, Graus F, Giometto B, et al: Central nervous system neuronal surface antibody associated syndromes: review and guidelines for recognition. J Neurol Neurosurg Psychiatry 2012; 83:638– 645 7. Tüzün E, Dalmau J: Limbic encephalitis and variants: classification, diagnosis and treatment. Neurologist 2007; 13:261–271 8. Barajas RF, Collins DE, Cha S, et al: Adult-onset drug-refractory seizure disorder associated with anti-voltage-gated potassiumchannel antibody. Epilepsia 2010; 51:473–477 9. Irani SR, Alexander S, Waters P, et al: Antibodies to Kv1 potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan’s syndrome and acquired neuromyotonia. Brain 2010; 133:2734– 2748 10. Vincent A, Buckley C, Schott JM, et al: Potassium channel antibodyassociated encephalopathy: a potentially immunotherapy-responsive form of limbic encephalitis. Brain 2004; 127:701–712 11. Malter MP, Helmstaedter C, Urbach H, et al: Antibodies to glutamic acid decarboxylase define a form of limbic encephalitis. Ann Neurol 2010; 67:470–478 12. Bien CG, Urbach H, Schramm J, et al: Limbic encephalitis as a precipitating event in adult-onset temporal lobe epilepsy. Neurology 2007; 69:1236–1244 13. Radja GK, Cavanna AE: Treatment of VGKC complex antibodyassociated limbic encephalitis: a systematic review. J Neuropsychiatry Clin Neurosci 2013; 25:264–271 14. Paterson RW, Zandi MS, Armstrong R, et al: Clinical relevance of positive voltage-gated potassium channel (VGKC)-complex antibodies: experience from a tertiary referral centre. J Neurol Neurosurg Psychiatry 2014; 85:625–630 15. Frisch C, Malter MP, Elger CE, et al: Neuropsychological course of voltage-gated potassium channel and glutamic acid decarboxylase antibody related limbic encephalitis. Eur J Neurol 2013; 20: 1297–1304 16. Ohshita T, Kawakami H, Maruyama H, et al: Voltage-gated potassium channel antibodies associated limbic encephalitis in a patient with invasive thymoma. J Neurol Sci 2006; 250:167–169 17. Dalmau J, Gleichman AJ, Hughes EG, et al: Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol 2008; 7:1091–1098 18. Moeller JJ, Friedman D, Dugan P, et al: Refractory status epilepticus associated with anti-SSA (anti-Ro) antibodies. Can J Neurol Sci 2012; 39:660–663 19. Johnson N, Henry C, Fessler AJ, et al: Anti-NMDA receptor encephalitis causing prolonged nonconvulsive status epilepticus. Neurology 2010; 75:1480–1482 20. Irani SR, Michell AW, Lang B, et al: Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Ann Neurol 2011; 69:892–900 21. Fernandez A, Claassen J: Refractory status epilepticus. Curr Opin Crit Care 2012; 18:127–131 22. Liimatainen S, Kai L, Johanna P, et al: Immunological perspectives of temporal lobe seizures. J Neuroimmunol 2013; 263:1–7 23. Shin YW, Lee ST, Shin JW, et al: VGKC-complex/LGI1-antibody encephalitis: clinical manifestations and response to immunotherapy. J Neuroimmunol 2013; 265:75–81 24. Thieben MJ, Lennon VA, Boeve BF, et al: Potentially reversible autoimmune limbic encephalitis with neuronal potassium channel antibody. Neurology 2004; 62:1177–1182 25. Andrade DM, Tai P, Dalmau J, et al: Tonic seizures: a diagnostic clue of anti-LGI1 encephalitis? Neurology 2011; 76:1355–1357 26. Dewolfe JL, Szaflarski JP: Levetiracetam use in the critical care setting. Front Neurol 2013; 4:121 27. Swisher CB, Doreswamy M, Gingrich KJ, et al: Phenytoin, levetiracetam, and pregabalin in the acute management of refractory status epilepticus in patients with brain tumors. Neurocrit Care 2012; 16:109–113 neuro.psychiatryonline.org

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J Neuropsychiatry Clin Neurosci 27:2, Spring 2015

Levetiracetam effect on adult-onset temporal lobe epilepsy with positive voltage-gated potassium channel antibody.

Temporal lobe epilepsy is considered to be the most frequent of all epileptic syndromes. Recently, several retrospective studies suggest that limbic e...
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