eMedicine Specialties > Neurology > Neurotoxicology

Cocaine: Differential Diagnoses & Workup

Author: Pinky Agarwal, MD, Clinical Assistant Professor, Department of Neurology, University of Washington; Attending Neurologist, Booth Gardner Parkinson's Care Center
Coauthor(s): Souvik Sen, MD, MS, FAHA,, Associate Professor of Neurology, Founding Director of UNC Hospital Stroke Center, Director of Neurovascular Residency, Department of Neurology, University of North Carolina at Chapel Hill
Contributor Information and Disclosures

Updated: Aug 26, 2009

Differential Diagnoses

Abnormal Neonatal EEG
Frontal Lobe Epilepsy
Anterior Circulation Stroke
Posterior Cerebral Artery Stroke
Basilar Artery Thrombosis
Seizures and Epilepsy: Overview and Classification
Cardioembolic Stroke
Simple Partial Seizures
Cerebellar Hemorrhage
Status Epilepticus
Cerebral Aneurysms
Subarachnoid Hemorrhage
Complex Partial Seizures
Confusional States and Acute Memory Disorders

Other Problems to Be Considered

Adrenergic crisis due to amphetamine overdose and thyroid storm (occasionally may mimic acute cocaine intoxication)
Cerebrovascular disease and stroke
Serotonin syndrome caused by antidepressant overdose may also look similar because of hyperactivity and hyperthermia.

Workup

Laboratory Studies

Lab tests should be ordered on the basis of patient presentation. Indications for ordering labs are as follows:

  • Diagnosis of cocaine use
    • Urine drug screen: Qualitative drug screens usually test for the inactive cocaine metabolite, benzoylecgonine, which may be present for as long as 36 hours after a single use. Metabolites can be demonstrated in the urine within 5 minutes after intravenous administration. With long-term use, urine metabolites may be detected for as long as 3 weeks after discontinuation of the drug. Urine drug screen in the neonate also can be used to detect possible in utero exposure to cocaine. The persistence of benzoylecgonine, which can be detected in the neonate's urine for as long as 4 days, is due to slow metabolism, probably related to immaturity or relative deficiency of plasma cholinesterases in the newborn.
    • Serum level of cocaine: This can be determined but has not been found to be useful clinically because of the rapid metabolism and short half-life of the drug.
  • Diagnosis of neurological complications: Tests used for diagnosing neurological complications include antinuclear antibody (ANA), creatine kinase (CK), CT scan, brain MRI, magnetic resonance angiography (MRA) of neck and intracranial vessels, 4-vessel angiogram, echocardiogram (transthoracic, transesophageal), positron emission tomography (PET), and single-photon emission computed tomography (SPECT).
  • CK: Urine should be evaluated routinely for the presence of myoglobin. Of patients with cocaine-induced rhabdomyolysis, 75% have a positive urine dipstick result for the orthotolidine reaction for heme, 67% yield positive findings for urine protein, and many manifest microscopic hematuria.

Imaging Studies

  • CT scan of brain: Focal neurological deficits or alterations in mental status are indications for performing CT scan of the brain. With long-term cocaine use, significant cerebral atrophy, enlarged lateral ventricles, and widened sylvian fissures may be seen. CT scan also reveals intracerebral hemorrhage.
  • MRI of brain: MRI of newborns exposed to cocaine in utero may reveal evidence of cortical infarction, major congenital malformations, and mainly midline CNS abnormalities. Prenatal cocaine exposure reveals subtle microstructural changes on diffusion tensor imaging, suggesting less mature development of frontal white matter pathways.7
  • MRA of brain and intracranial vessels: MRA is indicated in patients with ischemic stroke or subarachnoid hemorrhage. MRA may show evidence of vasculitis or aneurysm; venous phase may show evidence of venous thrombosis.
  • Four-vessel angiogram: This study is indicated in patients with a history of cocaine abuse and presenting with intracerebral hemorrhage, especially subarachnoid hemorrhage. Angiogram may show underlying vascular abnormalities. Berry aneurysms of the circle of Willis are a common finding. Arteriovenous (AV) malformations or tumor may be seen as well. Rarely, superior sagittal sinus thrombosis with hemorrhagic venous infarction, dural AV fistula, rupture of multiple mycotic aneurysms, and large-vessel thrombosis have been described. Angiographic beading can be seen in patients with vasculitis.
  • Neuroradiological study of newborns born to mothers who had used cocaine during pregnancy may reveal periventricular leukomalacia or holoprosencephaly. Evidence of intracerebral, intraventricular or subarachnoid hemorrhage may be observed. Sonography, CT scan, and MRI revealed cortical infarcts and midline congenital malformations in 15% of infants exposed to cocaine in utero.

Other Tests

  • ECG: Perform ECG if patient has chest pain.
  • EEG: Perform EEG in patients with seizures and a history of cocaine use. Habitual cocaine use can be associated with diffuse slowing on EEG. Focal abnormalities in the form of spikes or slowing can be seen in patients with focal seizures or intracerebral complications.
  • Transthoracic and transesophageal echocardiogram: Perform transthoracic and transesophageal echocardiogram in patients with embolic stroke caused by cocaine use. These studies may show evidence of vegetations in patients with infective endocarditis.
  • PET and SPECT: These studies may provide additional information in long-term cocaine users presenting with neuropsychiatric manifestations. Cerebral blood flow is reduced in habitual cocaine abusers, and abnormalities are most marked in the prefrontal cortex. Some investigators using PET have found reduced glucose metabolism over the entire cerebral cortex, thalamus, and midbrain. SPECT with iodine-123 isopropyl iodoamphetamine (IMP) revealed irregularly reduced cerebral perfusion even among asymptomatic social cocaine users who had normal findings on CT scans. In cocaine-dependent polydrug users (many of whom also used opioids and/or ethanol), some authors have found abnormal cerebral perfusion that primarily involved parietal, temporal, frontal, and basal ganglia.8
  • Ophthalmoscopic examinations and fundus photography of the retinas of cocaine addicts have revealed increased retinal arterial branching angle and venular caliber.9  

More on Cocaine

Overview: Cocaine
Differential Diagnoses & Workup: Cocaine
Treatment & Medication: Cocaine
Follow-up: Cocaine
References
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Further Reading

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Keywords

crack, street drugs, substance-related disorder, substance abuse, drug abuse, benzoylmethylecgonine, blow, coke, snow, toot, nose candy, freebase

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Contributor Information and Disclosures

Author

Pinky Agarwal, MD, Clinical Assistant Professor, Department of Neurology, University of Washington; Attending Neurologist, Booth Gardner Parkinson's Care Center
Pinky Agarwal, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, Association of Clinical Research Professionals, and Movement Disorders Society
Disclosure: Nothing to disclose.

Coauthor(s)

Souvik Sen, MD, MS, FAHA,, Associate Professor of Neurology, Founding Director of UNC Hospital Stroke Center, Director of Neurovascular Residency, Department of Neurology, University of North Carolina at Chapel Hill
Souvik Sen, MD, MS, FAHA, is a member of the following medical societies: American Academy of Neurology, American Heart Association, and Association for Patient Oriented Research
Disclosure: Nothing to disclose.

Medical Editor

Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
Edward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Neurological Association, American Society for Biochemistry and Molecular Biology, Phi Beta Kappa, Sigma Xi, Society for Neuroscience, and Southern Clinical Neurological Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard J Caselli, MD, Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale
Richard J Caselli, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Neurological Association, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Stephen A Berman, MD, PhD, Professor, Department of Internal Medicine, Section of Neurology, Dartmouth Medical School; Chief, Neurology Service, White River Junction Veterans Medical Center
Stephen A Berman, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

 
 
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