Spinal cord infarction in a young patient with methamphetamine abuse

Abstract

We report a case of a 20-year-old man who was diagnosed with spontaneous spinal cord infarction after abusing methamphetamine for a year. He presented with sudden onset of bilateral upper and lower limb weakness. His MRI spine showed a long segment of high signal intensity seen predominantly in the anterior spinal cord from medulla to mid thoracic level as well as a pencil-like hyperintensity seen postcontrast suggestive of spinal cord ischaemia or infarct. Thus, he was empirically treated for presumed anterior spinal cord infarction. He then developed autonomic dysfunction and went into respiratory distress, which required invasive mechanical ventilation support. Subsequently, he developed cardiac arrythmia with supraventricular tachycardiac followed by asystole and succumbed to illness on day 9 despite maximal resuscitative efforts. This case report illustrates a rare spinal cord infarction caused by methamphetamine intoxication and the importance of identifying and treating it early.

Background

Spinal cord infarction is a rare but often devastating disorder caused by a wide array of pathological states, likely spinal atherosclerotic thrombus, spinal artery embolism, fibrocartilaginous embolism, arteriovenous malformation, decompressive illness or traumatic events. Patients typically present with acute paraparesis or quadriparesis, depending on the level of the spinal cord involved. A key feature of the history is that the deficits usually reach nadir within 12 hours.¹ In addition, studies have shown that there is an increase in cases of spinal cord infarction due to substance abuse, mostly cocaine.^2–4 However, this case report is to alert clinicians that methamphetamine abuse can also cause spinal cord infarction and the importance of identifying and treating it early. In general, the diagnosis can be confirmed through neuroimaging findings, while laboratory investigations can help clinicians rule out other causes. Treatments provided are usually symptomatic, supportive and rehabilitative.

Case presentation

We report a case of a 20-year-old man who suffered from acute quadriparesis due to anterior spinal cord infarction secondary to methamphetamine abuse. He was fit and healthy previously but started abusing methamphetamine for the past 1 year, with a daily consumption of 0.1–0.2 mg of methamphetamine by insufflation (snorting). His initial symptoms were acute hand grip weakness, followed by bilateral upper and lower limb weakness and numbness. He had no history of trauma, photophobia, infection, urinary or bowel incontinence.

On arrival, he was alert and able to obey command, but his condition worsened after admission. His vital signs were labile, blood pressure was 80/50 mm Hg and required norepinephrine infusion. Clinical examinations revealed that he had lower motor neuron signs over bilateral upper and lower limbs. Generalised hypotonia and areflexia were observed, with power of all four limbs graded at 0/5. He had sensory impairment to pin prick touch all the way up to the level of C3–C4 dermatome, with intact proprioception. Cervical tenderness was present and his anal tone was lax. His pectoralis reflex was negative, bilateral plantar responses were unremarkable and he had no signs of meningism.

Urgent MRI was done on day 2 of admission. The MRI spine at Sagittal T2-weighted image (T2WI) view showed swelling of the spinal cord and long segment hypersignal intensity involving anterior segment of spinal cord from medulla to mid thoracic level (figure 1). Axial T2WI view showed hypersignal intensity involving anterior column and central grey matter, while posterior and lateral columns spared (figure 2). Moreover, at sagittal T1-weighted image (T1W1) postcontrast, it is also noted pencil-like hyperintensity involving the anterior segment of spinal cord from medulla to mid thoracic level (figure 3). However, his MRI and CT of brain were normal.

Figure 1.

Sagittal T2-weighted image. Swollen of the spinal cord and long segment hypersignal intensity involving anterior segment of spinal cord from medulla to mid thoracic level.

Figure 2.

Axial T2-weighted image. Hypersignal intensity involving anterior column and central grey matter and spared posterior and lateral column.

Figure 3.

Sagittal T1-weighted image postcontrast. Pencil-like hyperintensity involving the anterior segment of spinal cord from medulla to mid thoracic level.

Laboratory workup revealed that his full blood count, renal function, electrolytes, liver function test and coagulation profile were normal. His urine toxicology was positive for methamphetamine, but negative for barbiturates, cocaine, marijuana and opiates. On top of that, his hepatitis B, hepatitis C and HIV serology were negative. Blood and urine culture were also negative. Unfortunately, his family did not consent for lumbar puncture; therefore, we were unable to completely rule out infectious or inflammatory myelitis.

Intravenous methylprednisolone 500 mg was started with a possible diagnosis of idiopathic transverse myelitis. However, after thorough discussion with radiologists, we came to a consensus that he had an acute anterior spinal cord infarction involving the lower medulla to mid thoracic level (high cervical level lesion), which correlated to his sudden quadriparesis. MRI findings as described above are consistent with cord infarction rather than inflammation or infection. Therefore, we started him on antiplatelet and parenteral anticoagulation as empirical treatment. Methylprednisolone was stopped.

On day 4 of admission, he went into respiratory distress and required invasive mechanical ventilation support. His blood pressure and heart rate were persistently fluctuant, indicating autonomic dysfunction. A bedside echocardiography was carried out and showed no intracardiac thrombus. Unfortunately, his unstable condition prevented us from performing a second MRI spine to rule out new spinal cord embolism. We contemplated to put him on on-demand transcutaneous pacemaker in order to stabilise his heart rate, but ultimately he developed cardiac arrythmia with supraventricular tachycardiac followed by asystole and succumbed to his illness on day 9 despite maximal resuscitative efforts.

Investigations

MRI spine (figures 1–3).

Outcome and follow-up

He succumbed to his illness after treatment for 9 days in hospital.

Discussion

This case report shows a rare incidence of anterior spinal artery (ASP) infarction secondary to methamphetamine abuse. Spinal cord infarction is relatively uncommon and estimates of its occurrence are 1%–2% of ischaemic stroke and 5%–8% of all myelopathies.^5–7 Presentation can range from minor weakness to paraparesis and the onset can progress rapidly over minutes to hours.⁸ A thorough history and physical examination are crucial for rapid detection while MRI including sagittal and axial T1 and T2—weighted sequences, gadolinium sequences and diffusion-weighted imaging helps with confirmation and localisation of spinal cord infarction.^{1 8 9}

Methamphetamine is a known powerful, highly addictive stimulant that affects the central nervous system where it can be consumed by insufflation, smoking or intravenous injection.^{10 11} The common sympathomimetic effects are elevation of pulse rate and blood pressure, increased alertness and suppressed appetite. Common adverse events occurring as a result of vascular effects include myocardial infarction and stroke.^{12 13} Methamphetamine is also known to cause neurotoxicity and neuroinflammation.¹⁴ Thus, there are two major proposals to explain the mechanism of vascular effect causes by methamphetamine.¹⁵ First, the sympathomimetic effect of methamphetamines directly stimulates alpha and beta adrenergic receptors and simultaneously inhibits monoamine oxidase. When these events happen, they will cause an intense vasoconstriction, resulting in ischaemia distal to vessel.¹⁶ The second proposed mechanism is aseptic vasculitis with fibrinoid necrosis of the intima media with neutrophilic, eosinophilic and lymphocytic infiltration, which result in formation of a thrombus causing an ischaemia.¹⁷ In the present case, we are unable to pinpoint the exact pathogenesis of the spinal cord infarction, but its occurrence may suggest vasoconstriction and vasospasm in view of chronic methamphetamine abuse.

The methamphetamine molecule is structurally similar to amphetamine and to the neurotransmitter dopamine, a brain chemical that plays an important role in the reinforcement of rewarding behaviours, but it is quite different from cocaine.¹⁴ By comparing cocaine and methamphetamine, results showed that cocaine is quickly removed from and almost completely metabolised in the body, while methamphetamine has much longer duration of action and a larger percentage of the drug remains unchanged in the body.¹⁸ Therefore, methamphetamine remains much longer in the brain, which ultimately leads to prolonged stimulant effects, which makes it a drug with a higher potential for misuse.

The incidence of methamphetamine abuse causing spinal cord infarction is not well known. There are limited studies and case reports on the occurrence of this incident. Studies have shown that there is a higher preference and increased popularity of methamphetamine consumption as a club drug in the community.¹⁹ Therefore, we should be expecting more cases of methamphetamine abuse with the worst vascular complications, such as spinal cord infarction or ischaemic stroke. Cocaine abuse complicated with spinal cord infarction is more commonly reported as compared with methamphetamine abuse.^{2–4 20} In this case, the patient described above did sustain an anterior spinal cord infarction, with typical clinical and significant neuroimaging findings due to misuse of methamphetamine. However, the exact incidence is unknown.

Spinal cord infarcts can occur in the territories of the ASA or posterior spinal artery (PSA) or both.²¹ ASA syndrome typically presents with an abrupt onset of bilateral weakness, especially the lower limbs, sudden back pain, flaccid paraplegia, areflexia, loss of pain and, temperature sensations below the level of the lesion, sparing of proprioception and vibration sense (dissociative anaesthesia) and autonomic dysfunction involving the bladder and bowel.²² Infarcts in the territories of PSA are very rare.²³ The patients with PSA infarct usually present with signs of involvement of bilateral posterior columns, bilateral posterior horns and posterior segments of bilateral lateral columns.²⁴

The most common aetiologies of spinal cord infarct include spinal cord trauma, aortic surgery, vascular injury, arterial dissection, thromboembolic disease, atherosclerosis, vasculitis, hypercoagulable states or mass effect on the spinal cord and drugs.2 3 22 25 However, for this patient, we were unable to pinpoint the exact cause of his anterior spinal cord infarct because inadequate investigation was carried out to rule out infectious or inflammatory causes.

Cardiac arrhythmia is frequently observed in patients with spinal cord infarction and is generally considered to be caused by autonomic dysfunction. This is because the spinal sympathetic pathways that control the heart and maintain vascular tone exit at the first Q5 thoracic vertebra to fourth thoracic vertebra (T1–T4) levels, an unopposed parasympathetic tone may be present at the cervical or high thoracic (above T5) level in patients with SCI.^26–28 Atrial fibrillation, the most common sustained cardiac arrhythmia encountered in clinical practice with a prevalence of 1.0%–2.0% in the general population, can lead to substantial morbidity, reduced quality of life and increased mortality.^{29 30} Life-threatening bradycardia or sinus arrest requiring the implantation of a pacemaker has also been reported.³¹

Studies have shown that the severity and prognosis of spinal cord infarction depend on the level and the level of spinal cord involvement.^{32 33} Timely diagnosis and prompt management are essential to improve the outcome in most cases.³⁴ The aetiology of spinal cord infarction also plays a major role in determining the functional outcome.^32–34 However, there are not enough evidence to determine the prognosis of spinal cord infarction secondary to drug abuse. Therefore, we are unsure of the long-term outcome of these patients.

Learning points.

• Anterior spinal cord infarction can be caused by methamphetamine abuse.

• Spinal cord infarction is usually diagnosed clinically and confirmed by MRI.

• Treatment is usually symptomatic and supportive, while physical and occupational therapies may help improve the patients’ functional outcome.