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CASE REPORT

Lacunar Stroke Associated with
Methylphenidate Abuse
Hamid Sadeghian

ABSTRACT: Background: Methylphenidate is a central nervous system stimulant used for the
treatment of attention deficit hyperactivity disorder and narcolepsy and like other psychostimulants has
a potential for abuse. Case study: A young man with a cerebral lacunar infarction following chronic oral
abuse of methylphenidate is presented. Conclusions: The experience of our patient and a review of the
literature suggest that cerebral infarction is a potential side effect of chronic consumption of
methylphenidate.

RÉSUMÉ: Accident vasculaire cérébral associé à l’utilisation abusive de méthylphénidate. Introduction: Le
méthylphénidate est un stimulant du système nerveux central utilisé dans le traitement du syndrome
d’hyperactivité/déficit d’attention et de la narcolepsie et, comme d’autres psychostimulants, peut entraîner des abus.
Présentation de cas: Il s’agit d’un jeune homme qui a subi un infarctus cérébral lacunaire suite à l’abus oral
chronique de méthylphénidate. Conclusions: L’expérience de notre patient et une revue de la littérature suggèrent
que l’infarctus cérébral puisse être un effet secondaire de la consommation chronique de méthylphénidate.

Can. J. Neurol. Sci. 2004; 31: 109-111

Methylphenidate is a piperidine-derived central nervous
system (CNS) stimulant.1 It is commonly used for the treatment
of attention deficit hyperactivity disorder (ADHD) in children
and narcolepsy in adults.1 Some studies suggest possible
therapeutic uses for methylphenidate in elderly patients with
depression,2 patients with post-stroke depression,3 those with
traumatic brain injury,4 cancer patients,5 and those with human
immunodeficiency virus infection.6 This drug is related to
amphetamine and other psychostimulants. Methylphenidate
blocks the dopamine transporters in the presynaptic cell
membrane, leading to increased extra cellular levels of
dopamine.1,7,8 This mechanism is shared by amphetamine and
cocaine, which are well-known for their addictive properties and
neurologic complications following their abuse.7,9 The abuse
potential of methylphenidate is a problem that has received
considerable attention, especially in recent years.8,10,11 This
report describes a young man who suffered an ischemic stroke
following chronic methylphenidate abuse and suggests a causal
association between ingestion of methylphenidate and the
occurrence of cerebral infarction.

hydrochloride tablets 60 mg per day by mouth for the past six months.
He was not addicted to any other drug of abuse and denied using
methylphenidate by other routes.
General physical examination with emphasis on the cardiovascular
system showed no abnormalities. His blood pressure was 115/75 mmHg
at admission, and it never exceeded 130/80 mmHg during
hospitalization. There was no evidence of needle puncture, superficial
venous thromboses over the extremities, nasal mucosal ulceration or
septum perforation. At neurologic examination, mental state and speech
were normal. Cranial nerves were intact. There was a left central facial
palsy. Funduscopic examination showed a normal vascular pattern and
optic disc. There was no visual field defect. Right upper and lower
extremities had normal muscle tone and strength, whereas the left
extremities had decreased muscle tone. Left upper extremity strength
was 4+/5 both proximally and distally. Left lower extremity strength was
4/5 at proximal and 3/5 distally. Muscle bulk was normal. Muscle stretch
reflexes were diminished throughout on the left side in comparison to
right. There was no sensory loss or extinction. The plantar reflex was
upgoing on the left. There were no primitive reflexes. There was no
evidence of limb incoordination or cerebellar ataxia out of proportion to
weakness. He was not able to walk at the time of presentation.

CASE HISTORY
A 24-year-old university student suddenly developed left-sided
weakness without loss of consciousness while attending a class. His
weakness progressed over the next twenty minutes, then became fixed.
He was in good general health before the incident, had no significant
medical history and denied any similar symptoms in the past. His family
history was unremarkable and there were no risk factors for vascular
disease in his family members. He had used methylphenidate

From the Department of Neurology, Shahid Beheshti University of Medical Sciences
and Health Services, Tehran, Iran.
RECEIVED MARCH 26, 2003. ACCEPTED IN FINAL FORM AUGUST 21, 2003.
Reprint requests to: Hamid Sadeghian, Room UG 38, Neuromuscular Clinic,
Sunnybrook Center for Independent Living, Sunnybrook and Women’s College Health
Sciences Center, 2075 Bayview Avenue, Toronto, Ontario M4N 3M5 Canada

THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES

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https://doi.org/10.1017/S0317167100002924 Published online by Cambridge University Press

THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES

The following laboratory tests or investigations showed normal
results: complete blood count with differential; sedimentation rate;
blood chemistry and electrolytes, plasma homocysteine level, C-reactive
protein and lipid profile; serum protein electrophoresis; serum VDRL,
anti-HIV, anticardiolipin, antinuclear and ds DNA antibodies; serum
protein C, protein S, antithrombin III, factor V Leiden, and activated
partial thromboplastin time; liver enzymes; urinalysis; CSF analysis
including electrophoresis; ECG, chest x-ray, and transesophageal
echocardiography with intravenous bubble contrast.
Brain CT scan performed with and without injection of intravenous
contrast media showed a lacunar infarction involving the head of right
caudate nucleus and adjacent anterior limb of the internal capsule
(Figure). Magnetic resonance imaging (MRI) study as well as MR
angiography were not performed due to the patient’s severe
claustrophobia. Conventional four vessels cerebral angiography,
however, was normal. The course of recovery was uneventful and after
six weeks he was able to return to university. After neurologic
improvement, he was referred to a specialized facility for further
psychiatric evaluation and therapy.

DISCUSSION
Methylphenidate, like other psychostimulants, has a potential
for abuse, especially among student populations who use it for
nonmedical purposes.12 Abuse liability in controlled use of
methylphenidate for ADHD in children and adolescents, is
considered to be rare;7 however, illicit use occurs frequently
among middle and high school students without history of
ADHD.12,13 Most individuals abuse it for stimulant effects,

mainly wakefulness, suppression of appetite, increased
attentiveness and euphoria.
Although methylphenidate has been abused less frequently
than other CNS stimulants, a wide range of complications are
reported following its abuse, which in part depends on its route
of administration. This spectrum of complications differs from
side effects of therapeutic use of methylphenidate that includes
nervousness, headache, insomnia,14 and movement disorders.15
Methylphenidate has been abused intravenously,16 intraarterially,17 and intranasally18 using tablets crushed into powder,
in addition to oral route. Intravenous abuse of methylphenidate
has been followed by CNS toxicity with multiple organ failure,19
myelopathy,20 deep neck abscesses,21 and precocious
emphysema.22 Occasional fatal outcome has occurred following
intranasal abuse of methylphenidate.23
It is widely known that the chronic use of amphetamine,
among many other detrimental effects, may result in cerebral
vasculitis with consequent ischemic or hemorrhagic strokes.24,25
Ischemic and hemorrhagic stroke is also frequently seen in those
who use cocaine. These complications are presumably the result
of vasospasm caused by the sympathomimetic effects of cocaine
and induced hypertension.26 Other stimulants like phenylpropanolamine,27 methamphetamine28 and 3,4-methylenedioxymethamphetamine (Ecstasy)29 have also been incriminated as a
cause of cerebral vascular insults. Intravenous methylphenidate
can produce angiographic changes such as decreased vascular
diameter and filling defects in experimental models.30
A clinical report by Trugman31 described a patient with
hemidystonia, a few years after experiencing ischemic cerebral
infarction. The patient was diagnosed with ADHD at age five
and treated with methylphenidate 20 mg per day until age 12
when right hemiparesis and aphasia suddenly developed.
Cerebral angiography showed occlusion of the left anterior
cerebral artery and a branch of the left middle cerebral artery.
Brain MRI confirmed infarction in the left striatum and internal
capsule. Schteinschnaider et al32 reported an eight-year-old boy
with ADHD who developed repeated episodes of hemidystonia
and ataxia, while receiving methylphenidate 20 mg daily for 18
months. An MRI showed thalamic infarction and an angiogram
revealed occlusion of both posterior cerebral arteries.
The occurrence of lacunar infarction following chronic oral
abuse of methylphenidate in our patient who did not have any
known risk factor for cerebrovascular disease, suggests an
association between this drug and cerebral infarction. It is
possible that the observed lacunar infarct in the right caudate
nucleus is old and another infarct in the posterior limb of the
internal capsule, which is too small or too early to be seen in the
CT scan accounts for patient’s symptomatology. Nonetheless, it
seems justified to consider methylphenidate abuse as a potential
predisposing factor for stroke in this patient.
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Figure: Computerized tomographic scan shows a lacunar
infarction in the right caudate nucleus and adjacent part of
anterior limb of the internal capsule.

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