E Iacopini

A Clinical-EEG Study of Sleepiness and Psychological Symptoms in Pharmacoresistant Epilepsy Patients Treated with Lacosamide

Our aim was to evaluate the EEG and clinical modifications induced by the new antiepileptic drug lacosamide (LCM) in patients with epilepsy. We evaluated 10 patients affected by focal pharmacoresistant epilepsy in which LCM (mean 250 mg/day) was added to the preexisting antiepileptic therapy, which was left unmodified. Morning waking EEG recording was performed before (t0) and at 6 months (t1) after starting LCM. At t0 and t1, patients were also administered questionnaires evaluating mood, anxiety, sleep, sleepiness, and fatigue (Beck Depression Inventory; State-Trait Anxiety Inventory Y1 and Y2; Pittsburgh Sleep Quality Index; Epworth Sleepiness Scale; Fatigue Severity Scale). We performed a quantitative analysis of EEG interictal abnormalities and background EEG power spectrum analysis. LCM as an add-on did not significantly affect anxiety, depression, sleepiness, sleep quality, and fatigue scales. Similarly, adding LCM to preexisting therapy did not modify significantly patient EEGs in terms of absolute power, relative power, mean frequency, and interictal abnormalities occurrence. In conclusion, in this small cohort of patients, we confirmed that LCM as an add-on does not affect subjective parameters which play a role, among others, in therapy tolerability, and our clinical impression was further supported by evaluation of EEG spectral analysis.

Daytime sleepiness in de novo untreated patients with epilepsy

The aims of our study were to evaluate excessive daytime sleepiness in a group of de novo untreated people with epilepsy using a comprehensive and standardized approach, including subjective evaluation and neurophysiological and performance tests, and to compare these results with those obtained in a control group. Forty-seven patients with epilepsy (17 affected by primary generalized epilepsy and 30 by partial epilepsy), with a new epilepsy diagnosis and never treated, and 44 controls underwent Multiple Sleep Latency Test (preceded by nocturnal polysomnography), simple/complex visual reaction times, and Epworth Sleepiness Scale evaluation. Newly diagnosed and drug-free patients with epilepsy did not differ from controls in any of the tests performed to evaluate daytime sleepiness. In clinical practice, daytime sleepiness is a well-known and frequent complaint of patients with epilepsy, but different mechanisms and causes, such as associated psychiatric or sleep disorders, nocturnal seizures, sleep fragmentation, and antiepileptic drugs, must be taken into account. Excessive daytime sleepiness should not be considered an unavoidable consequence of epilepsy. Thus, a complete diagnostic work-up in patients with epilepsy and sleepiness should be undertaken whenever possible.

Exacerbation of restless legs syndrome presenting as a psychiatric emergency

Sir, We read with great interest the case descriptions by Mehta et al. [1] and Manconi and Fulda [2] and appreciated the highlight on restless legs syndrome (RLS) as a clinical manifestation in emergency. We report a similar, although less dramatic, case. We evaluated in the emergency department a 60-year-old male referred for severe worsening of RLS lasting continuously for 2 days and leading to severe insomnia and leg restlessness. The patient had a history of bipolar depression and impulse control disorder and was treated with valproate 900 mg/day. RLS symptoms started 2 years before but, since they were mild and sporadic, no treatment was suggested. Owing to severe insomnia and worsening of depressive symptoms, mirtazapine 30 mg at bedtime was added. Immediately after, RLS symptoms dramatically worsened. On the second night, pramipexole 0.25 mg in the evening was started with no benefit. In the third afternoon the patient came to the emergency department with severe agitation and restlessness, being unable to sit down without moving. We immediately decided to stop mirtazapine and, due to the anxiety symptoms and previous psychiatric history, we preferred not to use high dosage dopamine agonists and shifted the treatment to tramadol 25 mg and gabapentin 300 mg. The patient refused to be admitted into our ward. However, the next morning he reported an impressive improvement of the symptoms. In the first month, tramadol was gradually discontinued and gabapentin was increased to 600 mg/day. After more than 4 years of follow-up, RLS and bipolar symptoms appear still controlled with gabapentin 600 mg in the evening, valproate CR 300 mg TID and imipramine 12.5 mg TID. This case report is a further example of how RLS could become a real emergency. A drug-related worsening, or occurrence, of RLS symptoms should always be considered in the differential diagnosis of agitation. In this case, although psychiatric history and symptoms of anxiety were confounding factors, correct identification of RLS symptoms (both during the previous years and currently) together with a recent change in antidepressant therapy led to the correct diagnosis. The successful treatment was based on therapy with alpha-delta ligand, but probably even more so on the discontinuation of mirtazapine. It should be underlined that mirtazapine has the highest risk for RLS among second-generation antidepressants [3], typically within the first week, and provokes periodic limb movements even in healthy subjects [4]. However, a similar case report had been described with citalopram [5]. Thus, we would suggest that a list of contraindicated drugs should be diffused to general practitioners, other specialists and also to patients to help the correct treatment of comorbidities in RLS.