# Spastic Paraparesis Following Cocaine Inhalation

Authors: Henry Oluwasefunmi Savage; Malin Roesner; David Cohen
Journal: Case Reports in Medicine
 (2009)

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## Abstract

Cocaine use is reaching epidemic proportions in the UK and the consequences are a number of debilitating effects. Strokes may result from a number of mechanisms related to cocaine use. This report describes a case of cocaine induced stroke in an apparently healthy young man with unusual patterns of radiological findings on his brain MRI.


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## Body

## 1. Introduction

Cocaine dependence is
an enormous public health problem due to its vast array of medical complications.
Cerebral ischaemia is a recognized neurovascular effect of cocaine use. We
report the case of a young gentleman who presented with spastic paraparesis
shortly after cocaine inhalation and an unusual pattern of ischaemia seen on
magnetic resonance imaging of his brain.


## 2. Case Report

A 27-year-old male Caucasian
presented with sudden onset paraparesis. He had been on a social night out and
admitted to nasal inhalation of small quantities of cocaine about an hour
before onset of symptoms. There was no significant past medical history of note,
and he took no regular medication. He however admitted to recreational
consumption of cocaine for a few years.Clinical examination
revealed a regular heart rate of 90 beats per minute and an elevated blood
pressure of 148/70 mmHg. A 12-lead ECG performed was normal sinus rhythm with no
evidence of ischaemia. He had a right Horner sign, and there was grade1 power in
both legs with increased tone and brisk reflexes. Babinski sign was positive bilaterally.
Sensory examination was normal. The rest of his cranial nerve examination was
unremarkable. His Glasgow coma scale was 14/15, losing 1 verbal point due to
his mild confusion. He was however of normal GCS by the following day, 12 hours
later.Because of his
clinical presentation, an urgent magnetic resonance image of his spine was
performed initially which surprisingly did not reveal any abnormality. As a
consequence, the radiologist on discussion with the medical team proceeded to MRI
of his brain which demonstrated extensive subcortical white matter parasagittal
cerebral infarcts with focal lesions seen involving the
globus pallidus bilaterally, corpus callosum, and the right cerebellar
hemisphere (See Figure1). A urine sample was
positive for opiates and cocaine. Our patient categorically denied opiod use,
and the team agreed that this may have been a false positive test.Figure 1
T1/T2 weighted MRI
images showing parasagittal infarcts.Full blood count and
electrolytes were unremarkable and an autoimmune screen was negative. His
fasting blood sugar and lipid profile was normal. Cerebral arteriography and
venography were normal. Echocardiography demonstrated a patent foramen ovale; however,
doppler ultrasound of the deep veins of his legs revealed no thrombosis. A 12-lead electrocardiograph revealed sinus rhythm.He was managed on our
stroke unit, receiving intensive neurorehabilitation and regaining mobility
with crutches after 12 days. A cardiology review concluded that there were no
compelling indications for closure of his atrial septal defect in view of a
probable cause of his stroke. His blood pressure throughout his admission was
normal. He was thus discharged home after 2 weeks of inpatient stay with a
referral to his local drug and alcohol abuse service. He has so far made a
complete recovery.


## 3. Discussion

Cocaine remains a
common non alcoholic drug of abuse in the United Kingdom, and this seems to be
on the rise. Its use along with other drugs of abuse continues to pose a
serious public health problem. There were 162 203 drug users in contact with drug treatment
services and GPs for 2008 in the UK [1].The UK has the highest adult prevalence of both lifetime and recent cocaine
use in Europe, and levels of use among younger adults and people who lived in
urban areas tended to be higher than the population average [2]. The
most recent data available puts the lifetime prevalence of cocaine use for the UK
adult population at 7.7% (i.e., have used at least once). The range of lifetime experience among European 15- to 34-year-olds
is between 0.4% and 11.2%, and the UK is also at the top of this range [2].Acute cocaine toxicity
may result in ischaemic or hemorrhagic strokes. A variety of neuropsychiatric
complications are also well recognized [3, 4].Cocaine is thought to cause strokes through various proposed mechanisms.
This includes global cerebrovasospasm as a result of its potent vasoconstrictor
ability which may lead to global cerebral hypo perfusion. Dose-related cerebral vasoconstriction on magnetic resonance angiograms has been
observed [5]. Cocaine prevents the reuptake of noradrenaline,
serotonin and dopamine at pre-synaptic nerve terminals. It may also act directly on the vascular smooth muscle cells by direct effects on
calcium channels, promoting intracellular calcium release from the
sarcoplasmic reticulum. There is post mortem evidence to support vasospasm with consistent
histological findings
in nasal arterioles [6], intestinal arterioles [7], and coronary
arteries [8].Cocaine may disrupt cerebral auto-regulation and is found to reduce cerebral
blood flow in users as found by Volkow et al. [9] and a Californian
group [10]. There is also evidence to suggest reduced metabolism
following cocaine administration which may also result in down regulating
cerebral blood flow [11].Atherosclerosis is an important consequence of cocaine use, and this has
been demonstrated in the cerebral vasculature. The mechanism of atherosclerosis
is thought to relate to vascular injury from vasospasm leading to endothelial
injury and the consequence of thrombus formation. Increased platelet
aggregation may also play a part.In vivo studies have demonstrated increased platelet aggregation
secondary to cocaine administration [12]. This mechanism of causing
strokes is important because even in the absence of atherosclerotic disease or
vascular endothelial damage thrombus formation is possible.An inflammatory vasculopathy may result
from cocaine use but this is less common. The basis of cerebral vasculitis has
been attributed to angiographic findings of vessel
necrosis and arterial beading [13].Cardioembolism is another important cause of strokes from embolised
impurities either  in patients who utilize the intravenous route or in those who suffer
cocaine-related MI and arrhythmias or develop cardiomyopathies [14]. It is
important to continue to follow these patients up.The extensive and symmetrical pattern of
subcortical infarcts noted in the parasagittal region in our patients MRI is an
unusual finding, and these lesions were clearly related to their dramatic symptoms
at presentation.In view of his presentation immediately
post inhalation of the drug and mild abnormality of his GCS, we theorised that
our patient may have been a victim of sudden onset global cerebrovasospasm. This,
we believed, resulted in focal damage to both large and small cerebral vessels.It
is conceivable to associate the pattern of injury in our patient to the variety
of proposed mechanisms of cocaine-related cerebrovascular injury. The
possibility of cardioembolism via his patent foramen ovale remained present;
however, our patient-denied intravenous use of drugs and certainly did not have
any obvious clinical signs to the contrary. Other investigations were unable to
conclusively identify any other mechanisms that may have been contributory, even
though our patient had radiological evidence of some diffuse disease.We monitored his blood pressure through admission
which was consistently normal and thus did not treat for hypertension. On
discharge, we recommended that his general practitioner follow this up. There
were no other risk factors for cerebrovascular disease identified.In conclusion, with the seemingly upward
trend in cocaine consumption in the UK, it is important to recognize the
possible presentations of cocaine-induced cerebrovascular disease. It remains
necessary to identify other risk factors for cerebrovascular disease in these
patients. Ultimately, making a prompt diagnosis and offering such patients
immediate treatment and long-term management in terms of counselling and
contact with drug treatment services may improve their lives.



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