We present a case of cervical myoclonias probably associated with Etanercept.
A 16-year-old woman, diagnosed with severe plaque psoriasis, under dermatological follow-up and on treatment with Etanercept 25 mg twice a week. She consulted for abnormal cervical movements in March 2013. She had started treatment with etanercept 25 mg twice weekly in May 2012 for a flare-up of severe plaque psoriasis that did not respond to topical (clobetasol, calcipotriol, betamethasone + calcipotriol) and oral (ciclosporin and mycophenolate mofetil) treatments. After 12 weeks of treatment, a complete clinical response was achieved and the drug was withdrawn. One week after the last dose of etanercept, administered on 29 June 2012, he developed granulomatous interstitial dermatitis of the extremities, which was attributed to the withdrawal of etanercept6. In November 2012, she had a new flare-up of psoriasis, and the severity was assessed using the Psoriasis Area and Severity Index (PASI) calculation, with a PASI of 18.60. Etanercept 25 mg twice weekly was restarted and clinical improvement was achieved after 15 weeks of treatment.
On 5 March 2013, the patient was admitted to Internal Medicine for a 48-hour history of sudden, involuntary, repetitive, arrhythmic and sustained movements of the head to the left during sleep. He had received the last dose of etanercept on 27 February 2013. The condition was not accompanied by any other systemic symptoms. The movements caused twitching of the left upper limb, were painless and associated with hypoaesthesia in the hemiface and anterior portion from D4 to L2. She did not report similar previous episodes or movement alterations at these or other levels suggesting a personal history of myoclonus, dystonia or any other type of involuntary movement. On physical examination he was afebrile and haemodynamically stable. The neurological examination revealed nociceptive hypoaesthesia in the left hemiface and anterolateral part of the trunk from D2 to L2, and D2 to D8 in the back.
Among the complementary tests, an electroencephalogram was performed, showing myoclonic movements of left cervical flexion and elevation of the left shoulder, presenting over the temporoparietal region of the same hemisphere a graphoelement with a spike morphology that precedes the movement by 200-400 ms, interpreted as an artefact due to muscle contraction.
In view of the clinical suspicion of AMR due to Etanercept, the drug was withdrawn and an exhaustive search was requested from the hospital's Pharmacy Service on the reactions described with Etanercept.
Treatment was started with carbamazepine 100 mg for suspected paroxysmal dyskinesias, which was discontinued due to dizziness and nausea. Subsequently, treatment was prescribed with clonacepam 0.5 mg 1-1-2, levitiracetam 250 mg c/12 h, valproic acid 500 mg c/8 h and diazepam 2.5 mg 0-1-2 without improvement. A differential diagnosis was made between spinal myoclonias, although without long tract involvement, paroxysmal non-kinesiogenic dyskinesias or dystonia-myoclonias. One week after admission, the clinical picture began to respond with diazepam at doses of 2.5 mg 1-1-2, clonazepam 0.5 mg 1-1-2, valproic 500 mg c/8 h, levetiracetam 1000 mg c/12 h and biperidene 2 mg c/8 h. On the tenth day, the patient was discharged from the hospital. On the tenth day she was discharged with clinical improvement and treatment with clonazepam 0.5 mg 1-1-2, biperiden 4 mg c/24 h and levetiracetam 1000 mg c/12 h in a descending regimen.