We report a case of cervical myoclonus probably associated with Etanercept.
A 16-year-old woman diagnosed with severe plaque psoriasis was followed up by dermatology and treated with Etanercept 25 mg twice a week.
She presented abnormal cervical movements in March 2013.
She had started treatment with etanercept 25 mg twice a week in May 2012, due to a bud of severe plaque psoriasis that did not respond to topical treatments (clobetasol, calcipotriol, betamethasporotide + oral).
After 12 weeks of treatment a complete clinical response was obtained and the drug was withdrawn.
One week after the last dose of etanercept, administered on June 29, 2012, the patient developed interstitial granulomatous dermatitis in the extremities, which was attributed to etanercept withdrawal.
In November 2012, there was a new sprout of psoriasis, severity was assessed by calculating the Psoriasis Area and Severity Index (PASI), obtaining a PASI index of 18.60.
Etanercept 25 mg twice weekly was restarted, achieving clinical improvement after 15 weeks of treatment.
On March 5, 2013, the patient was admitted to Medicine due to a 48-hour history of sudden, involuntary movements of the head toward the left internal sleep and maintained arrhythmic internal sleep.
He had received the last dose of etanercept on February 27, 2013.
The clinical picture was not accompanied by any other systemic symptoms.
The movements provoked saccades of the left upper limb, were painless and associated hypoesthesia in the anterior hemisphere and portion from D4 to L2.
He did not report similar previous episodes or movement alterations at these or other levels that suggested a personal history of myoclonus, dystonia or any other type of involuntary movement.
Physical examination revealed fever and hemodynamically stable.
Neurological examination revealed left hemiblock hypoesthesia and anterolateral trunk hypoesthesia from D2 to L2, and from D2 to D8 on 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 with a spike-eckle motion interpretation ms.
Because of the clinical suspicion of ADR by Etanercept, the drug was withdrawn and an exhaustive search was requested from the hospital emergency department about the reactions described with Etanercept.
Carbamazepine 100 mg was started due to suspicion of paroxysmal dyskinesias and was discontinued due to dizziness and nausea.
Treatment 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 were successively discontinued.
A differential diagnosis was proposed between spinal myoclonus, although without long pathway involvement, non-kinesthetic paroxysmal dyskinesias or dystonia-myoclonus.
At the week of admission, the patient developed 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.
The tenth day 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 descending order.
