Acute neurologic and psychiatric complications associated with cocaine abuse

doi:10.1016/0002-9343(87)90640-1

The American Journal of Medicine

Volume 83, Issue 5, November 1987, Pages 841-846

https://doi.org/10.1016/0002-9343(87)90640-1 Get rights and content

Abstract

This report reviewed 996 emergency room visits and 279 hospital admissions of patients with complications of cocaine abuse seen at the San Francisco General Hospital between 1979 and 1986. In 143 cases, acute neurologic or psychiatric symptoms were the primary complaint, and case-notes provided sufficient detail for analysis. The major neurologic complications included one or more seizures (n = 29), focal neurologic symptoms or signs (12), headache (10), and transient loss of consciousness (six). Psychiatric disturbances included agitation, anxiety, or depression (33), psychosis and paranola (24), and suicidal ideation (18). The most serious consequences were found in patients with prolonged seizures or strokes, those who jumped out of buildings, and those who attempted suicide by overdosing with other drugs. There was no correlaton between the appearance of complications and the reported route of administration, the amount of cocaine used, or prior experience with cocaine. The number of patients who are seeking hospital attention for these or related complaints appears to be rising substantially. Cocaine abuse, regardless of the use pattern, is associated with a variety of potentially severe neurologic and psychiatric complications.

References (35)

VJM Di Maio et al.
Four deaths due to intravenous injection of cocaine
Forensic Sci Int
(1978)
DW Mathias
Cocaine-associated myocardial ischemia: review of clinical and angiographic findings
Am J Med
(1986)
H Lesse et al.
Effects of cocaine on propagation of limbic seizure activity
Pharm Biochem Behav
(1979)
H Lesse et al.
Differential effects of cocaine on limbic excitability
Pharmacol Biochem Behav
(1980)
AA Nanji et al.
Asystole and ventricular fibrillation associated with cocaine intoxication
Chest
(1984)
JA Myers et al.
Generalized seizures and cocaine abuse
Neurology
(1984)
KA Schwartz et al.
Subarachnoid hemorrhage precipitated by cocaine snorting
Arch Neurol
(1984)
PJ Lichtenfeld et al.
Subarachnoid hemorrhage precipitated by cocaine snorting
Arch Neurol
(1984)
LI Golbe et al.
Cerebral infarction in a user of free-base cocaine (“crack”)
Neurology
(1986)
CV Wetli et al.
Cocaine-induced psychosis and sudden death in recreational cocaine users
J Forensic Sci
(1985)

TW Estroff et al.

Medical and psychiatric complications of cocaine abuse with possible points of pharmacological treatment

Adv Alcohol Subst Abuse

(1985)

S Freud

The cocaine papers

(1963)

E Pulay

Cocaine poisoning

JAMA

(1922)

E Mayer

The toxic effects following the use of local anesthetics

JAMA

(1924)

CV Wetli et al.

Death caused by recreational cocaine use

JAMA

(1979)

CA Suarez et al.

Cocaine-condom ingestion: surgical treatment

JAMA

(1977)

JM Isner et al.

Acute cardiac events temporally related to cocaine abuse

N Engl J Med

(1986)

Cited by (197)

Approach to toxicological deaths
2022, Principles of Forensic Pathology: From Investigation to Certification
Drug intoxication deaths are encountered with increasing frequency in medicolegal death investigations. An examination of the scene may yield critical information that suggests a drug intoxication. The autopsy examination is a critical part in the investigation of a potential death due to a drug intoxication. At autopsy, blood (cardiac and femoral), vitreous humor, and urine are standard toxicology specimens. Blood should be collected in a sodium fluoride (Na–F)-containing tube to prevent the in vitro enzymatic breakdown of cocaine and the production of ethanol. Cocaine, opioids (fentanyl, heroin), and stimulants (cocaine) are further discussed, as are issues encountered in toxicologic suicides. Postmortem changes can result in the alteration of various drugs and their concentrations from what was present at the time of death. In order to certify a death as due to a drug intoxication, there are three considerations: (1) the history and scene are consistent with a drug intoxication death, (2) the autopsy fails to disclose a more compelling disease or physical injury with a severity that is inconsistent with continued life, and (3) the toxicological concentrations are in the range typically encountered in such deaths.
Stroke and Substance Abuse
2021, Stroke: Pathophysiology, Diagnosis, and Management
A number of recreationally used drugs, licit and illicit, have been linked to ischemic and hemorrhagic stroke. In some cases, for example, ethanol and tobacco, epidemiologic data convincingly identify the agents as risk factors without implying direct temporal causality. In the case of psychostimulant drugs-including methamphetamine, 3,4-methylenedioxymetamphetamine ("ecstasy"), cathinone derivatives ("bath salts"), and cocaine, as well as cannabis products-linkage is based on case reports and limited epidemiologic data, but temporal association of use, plus biological plausibility, suggest direct causality. Recreational drug use should be considered in any patient with a stroke, regardless of age.
Headache in Cocaine Users: Epidemiology, Clinical Features, and Putative Pathophysiological Mechanisms
2017, The Neuroscience of Cocaine: Mechanisms and Treatment
Headache is a frequent symptom in cocaine users (CUs). Chronic cocaine use may induce headache in previously unaffected individuals or worsen a preexisting headache. Cocaine-induced headache is usually migraine-like, and less commonly tension type- or cluster-like. The latency between acute cocaine use and headache onset ranges from minutes to several days. Cocaine-induced headache, as currently defined, develops ≤1 hour after cocaine administration and subsides ≤72 hours later. Given that headache often begins 2–12 hours after cocaine use these criteria remain open to debate. Acute cocaine use commonly worsens spontaneous migraine attacks, and rarely improves cluster episodes. Putative pathophysiological headache mechanisms in CUs include massive sympathomimetic stimulation followed by monoamine depletion, increased glutamatergic activity, and trigeminal or sphenopalatine ganglia activation. Being aware about headache in CUs is important so that we can manage this complication properly and treat patients adequately. Understanding more about the underlying mechanisms should also improve our knowledge of headache pathophysiology.
Stroke and Substance Abuse
2015, Stroke: Pathophysiology, Diagnosis, and Management
Neurologic complications of psychomotor stimulant abuse
2015, International Review of Neurobiology
Citation Excerpt :
In the remaining four patients, the seizures were secondary to postanoxic encephalopathy, stroke, brain contusion, or alcohol withdrawal. A similar low incidence of seizures was reported based on a review of emergency room visits and hospitalizations (Lowenstein et al., 1987). Generalized seizures occurred in 2.3% of the patients; they occurred in 1.6% of patients within 12 h of cocaine use.
Psychomotor stimulants are drugs that act on the central nervous system (CNS) to increase alertness, elevate mood, and produce a sense of well-being. These drugs also decrease appetite and the need for sleep. Stimulants can enhance stamina and improve performance in tasks that have been impaired by fatigue or boredom. Approved therapeutic applications of stimulants include attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity. These agents also possess potent reinforcing properties that can result in excessive self-administration and abuse. Chronic use is associated with adverse effects including psychosis, seizures, and cerebrovascular accidents, though these complications usually occur in individuals with preexisting risk factors.
This chapter reviews the adverse neurologic consequences of chronic psychomotor stimulant use and abuse, with a focus on two prototypical stimulants methamphetamine and cocaine.
A systematic review of evidence on the association between cocaine use and seizures
2013, Drug and Alcohol Dependence
Citation Excerpt :
They are divided into three categories according to their study population and study design. The prevalence of seizures in the 11 selected studies of patients who were either hospitalized or who presented to emergency rooms due to cocaine use ranged between 0.9% and 10.4% (Anta et al., 1998; Blaho et al., 2000; Brody et al., 1990; Choy-Kwong and Lipton, 1989; Derlet and Albertson, 1989; Dhuna et al., 1991; Lowenstein et al., 1987; Pascual-Leone et al., 1990; Rich and Singer, 1991; Sanjurjo et al., 2006; Sopena et al., 2008). These studies found no major differences in the prevalence of seizures between patients who were hospitalized for cocaine use and those who attended emergency rooms for cocaine use.
Institutional monographs/medical textbooks mention seizures as a neurological complication of cocaine, but no systematic reviews (SRs) have been published on this issue. We aimed to conduct a SR of the literature on the relationship between cocaine use and seizures and to summarize the biological plausibility of that relationship.
The pathophysiological mechanisms that may underlie an association between cocaine and seizures were summarized; a SR was then performed using three databases (EMBASE, Medline, PsycINFO) and the Cochrane-library to search for published papers (1980–2012) aimed at quantifying the associations between cocaine use and seizures. The inclusion criteria for selection were: articles based on clinical trials, cohort, case-control (CC) or cross-sectional (CS) studies, participants ≥14 years old and not pregnant, and use of cocaine in the last 72 h. Information was extracted, evaluated and cross-checked independently by two researchers.
Of the 1243 potentially relevant articles initially identified; one CC and 22 CS studies were finally selected. The CC study did not find cocaine use to be a risk-factor for seizures. In addition to the limitations of the CS design, these studies had important methodological weaknesses and biases.
Despite its biological plausibility, no rigorous scientific evidence supports a causal relationship between cocaine use and seizures. The misinterpretation of the role of cocaine may have important implications in medical services. Well-conducted studies are urgently needed.

View all citing articles on Scopus

View full text

Clinical studiesAcute neurologic and psychiatric complications associated with cocaine abuse

Abstract

Forensic Sci Int

Am J Med

Pharm Biochem Behav

Pharmacol Biochem Behav

Chest

Generalized seizures and cocaine abuse

Neurology

Subarachnoid hemorrhage precipitated by cocaine snorting

Arch Neurol

Subarachnoid hemorrhage precipitated by cocaine snorting

Arch Neurol

Cerebral infarction in a user of free-base cocaine (“crack”)

Neurology

Cocaine-induced psychosis and sudden death in recreational cocaine users

J Forensic Sci

Medical and psychiatric complications of cocaine abuse with possible points of pharmacological treatment

Adv Alcohol Subst Abuse

The cocaine papers

Cocaine poisoning

JAMA

The toxic effects following the use of local anesthetics

JAMA

Death caused by recreational cocaine use

JAMA

Cocaine-condom ingestion: surgical treatment

JAMA

Acute cardiac events temporally related to cocaine abuse

N Engl J Med

Clinical studies
Acute neurologic and psychiatric complications associated with cocaine abuse