Case Summary
A 29‐year‐old woman with history of polysubstance abuse presented to the hospital after 5 days of lethargy and altered mental status. She was cachectic, hypomimic, and almost anarthric. She had extreme bradyphrenia, bradykinesia, and shuffling gait with en‐bloc turns. Strength and tone were normal, and reflexes were diffusely 3 + with flexor response to plantar stimulation. Extensive infectious, metabolic, and inflammatory/autoimmune workup was not revealing. Echocardiogram and MRA of head were negative. Brain MRI revealed evolving bilateral basal ganglia infarction with surrounding edema (Fig. 1). After drug screen revealed amphetamine positivity, she admitted to “crystal meth” use. Carbidopa/Levodopa led to only mild improvement in postural stability.
Figure 1.
(A) Diffusion weighted image demonstrates restricted diffusion of the caudate head. (B) Fluid‐attenuated inversion recovery axial MRI reveals abnormal hyperintensities involving bilateral basal ganglia involving the internal capsule and sparing the thalami. (C) Pre‐contrast and (D) post‐contrast axial T1‐weighted MRI demonstrate bilateral basal ganglia with gadolinium enhancement.
This case illustrates an uncommon, but devastating neurologic consequence of methamphetamine abuse. Methamphetamine can cause toxicity to nigrostriatal pathways. Being lipophilic, it readily crosses the blood‐brain barrier. It binds to dopamine, norepinephrine, and to a lesser extent, serotonin receptors. It induces monoamine release from synaptic terminals and decreases re‐uptake and enzymatic degradation. This can deplete dopamine neurons and potentially contribute to excitotoxicity, oxidative stress, and mitochondrial dysfunction.1 Additionally, it can induce focal arterial vasoconstriction or an inflammatory vasculitis, causing ischemic stroke.2 Methamphetamine use increases the risk of developing Parkinson disease.1 This patient had history of prior polysubstance abuse, and we cannot fully rule out that other toxic exposures contributed to her insult, but acute presentation in the context of positive urine drug screen made the case compelling. Awareness of this potential toxicity may aide appropriate diagnosis and counseling.
Author Roles
(1) Research Project: A. Conception, B. Organization, C. Execution; D. Supervision; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript: A. Writing of the First Draft, B. Review and Critique.
W.D.: 3A, 3B
J.Y.: 3A, 1B
I.M.: 3A, 3B
Disclosures
Ethics Compliance Statement: The authors confirm that the approval of an institutional review board was not required for this work. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.
Funding Sources and Conflicts of Interest: The authors report that no specific funding was received for this work; there are no conflicts of interest relevant to this work; and that there are no additional disclosures to report.
Financial Disclosures for Previous 12 Months: University of Florida for all authors.
Relevant disclosures and conflicts of interest are listed at the end of this article.
References
- 1. Rusyniak DE. Neurologic manifestations of chronic methamphetamine abuse. Psychiatr Clin North Am 2013;36(2):261–275. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Christensen MR, Lesnikova I, Madsen LB, Rosendal I, Banner J. Drug‐induced bilateral ischemic infarction in an amphetamine addict. Forensic Sci Med Pathol 2013;9(3):458–461. [DOI] [PubMed] [Google Scholar]