Abstract
Ritalin® (methylphenidate) is an amphetamine-like prescription stimulant commonly used in the treatment of attention deficit hyperactivity disorder in children and adults. Recently, the recreational use of Ritalin has increased, particularly among young adults. Well-known symptoms of intoxication include signs of sympathetic nervous stimulation, such as agitation, anxiety, tachycardia, hypertension, headache, tremor, and dizziness. This case report describes oral dyskinesia as a rare presentation of Ritalin intoxication, with the review of pathophysiology and some epidemiological data.
Case report
In this study, we present the case of a 19-year-old male brought to the emergency department (ED) for unintentional and persistent jaw and tongue movements. He had a friend who accompanied him to the ED and provided additional information. According to this friend, the two men went to a club in town, where the patient consumed about 2.5 L of beer and three drinks with vodka. He had also smoked marihuana earlier that evening. The friend called the ambulance when the patient started with unintentional jaw movements and became anxious that he had been drugged by someone else in the club. The paramedical staff found the patient with a Glasgow Coma Scale (GCS) of 15, agitated but with no neurological abnormalities. The patient’s history was unremarkable, except for a history of attention deficit hyperactivity disorder with intermittent use of Ritalin®, prescribed by his general physician (GP).
On arrival, the patient’s vital signs were stable, with a pulse of 115, respiration rate of 15, blood pressure of 120/90, and O2 saturation of 99%. Paramedical staff measured blood glucose of 6.5 mmol/L by pricking his finger.
On physical examination, the patient exhibited psychomotor agitation. His heart rate was regular and his pulse was strong. His lungs were clear to bilateral auscultation. His abdomen was soft, non-tender, and non-distended. The neurological examination found that the patient had a GCS of 15. His pupils were 1.5 mm in diameter and reacted promptly. The right and left eyes reacted similarly. The core temperature was 37.2°C.
The patient exhibited noticeable psychomotor restlessness, moving around constantly, with panic-like fear that he might collapse. The unintentional and persistent jaw and tongue movements reported by his friend were confirmed and could be partially suppressed by talking to the patient.
We obtained an electrocardiogram that showed a tachycardia sinus rhythm with rate of 105, normal axis, normal intervals, and no ST-wave abnormalities.
Patient’s blood sample has been sent to the laboratory for the following studies. His complete blood count revealed white blood cell count of 13.2 g/L, haemoglobin of 142 g/L, haematocrit of 0.42, and platelet count of 360 g/L. His international normalized ratio was 1.0. We measured cardiac markers, including creatine kinase and troponin, both of which were normal. His basic clinical chemistry was within normal limits, with base excess of −0.9. His respiratory alcohol level was 1.8 ppm. The urine drug screen was negative for all tested substances (including cocaine, amphetamines, and methamphetamines). His chest x-ray was normal.
The management in the ED was primary supportive. The patient was given 1000 mL intravenous bolus of normal saline. He was administered 2.5 mg of sublingual lorazepam, which gave a marked response within 30 min.
At that point, the results of the analysis of urine drug screening were available. The patient and his friend were again questioned about other possible drugs, including his Ritalin intake. The patient admitted to having ingested 60 mg of nasal Ritalin that evening, about 30 min before the symptoms began. He had never done that before, because his GP had prescribed the drug only 1 month earlier.
After another intravenous dose of lorazepam, the orofacial dyskinesia resolved completely and the patient could be discharged after a few hours of observation.
Discussion
Methylphenidate is a short-acting stimulant with duration of 1–4 h and a pharmacokinetic half-life of 2–3 h. Methylphenidate has two chiral centres, but the drug used in therapy comprises only the threo pair of enantiomers.
Neurologic side effects of methylphenidate are well known and include headaches, irritability, tics, chorea, psychosis, and, rarely, paroxysmal kinesigenic dystonia. 2 –4
The potential recreational use of methylphenidate has long been known, not least because of the relatively simple acquisition and pharmacodynamic similarities to other stimulants. The mechanisms of Ritalin and cocaine are virtually identical. The subjective response to acute ingestion is very similar to that of cocaine, 5 but the physiological response resembles to that of amphetamine. 6 Non-medical use is common and is increasing steadily. 7 The most common route of exposure is oral (about 60%), followed by intravenous and inhalation. 7 Acute overdoses of methylphenidate lead to dose-dependent sympathomimetic responses. 8
Drug-induced dyskinesias have been described in association with methylphenidate use and occur in two forms. Late dyskinesias are common and have been well described.2–4,8 Early onset dyskinesia is relatively rare and only seven cases have previously been described. 9 –14
This case report of early onset orofacial dyskinesia after nasal ingestion of Ritalin is of special interest because of the pharmacodynamic characteristics of the dyskinesia. The facial movements appeared immediately after nasal methylphenidate ingestion and subsided fairly rapidly within a few hours in an ‘on–off’ fashion. This abbreviated and demarcated onset and disappearance hints at the underlying neurologic mechanisms involved. Methylphenidate blocks dopamine transporters and – as an indirect dopamine agonist – increases extracellular dopamine level in the striatum. Balazs suggested that high serum levels of methylphenidate could hyperstimulate dopamine receptors and cause the early onset of the symptoms. 9
The rapid onset of the adverse effects was also favoured by the nasal ingestion leading to rapidly rising plasma concentrations and increased bioavailabilities for both enantiomers when compared with oral dosing. Furthermore, our patient’s preceding ethanol consumption might have interacted with the methylphenidate and led to altered pharmacokinetics and altered drug metabolism. It has been shown that in case of oral methylphenidate intake, the presence of ethanol in the body accelerates methylphenidate absorption leading to earlier t
max and higher C
max for
Our case report has practical implications for physicians who prescribe Ritalin to young adults, where it can serve to increase the awareness of non-medical use and draw attention to dyskinesia as a potential side effect.
Footnotes
Conflict of interests
The authors declared no conflicts of interest.