Chronic cocaine use results in increased impulsiveness along with deficits in learning, memory and decision-making. But can cocaine damage a person’s nerves and cause neuropathy?

Cocaine is a powerful central nervous system (CNS) stimulant that causes feelings of intense pleasure and increased short-term arousal. Cocaine produces these euphoric effects by increasing the activity of neurotransmitter systems that cause arousal. After a neurotransmitter is released, it is either deactivated by an enzyme or removed via reuptake by neurons. Cocaine blocks the reuptake of neurotransmitters like dopamine, serotonin and norepinephrine that are responsible for increased arousal.

Neuropathy refers to any condition that affects the regular activity of the nervous system. In the context of the central nervous system or the brain, cocaine addiction and withdrawal result in abnormal activation patterns at the systemic level (different brain pathways and brain regions), cellular level (functioning of different neurons) and molecular level (changes in gene expression patterns). 

Cocaine use gradually leads to tolerance, meaning that more and more of the drug is then needed to produce pleasurable effects. Chronic cocaine use results in cognitive deficits such as a decline in memory, drug dependence and the inability to feel pleasure. These changes are accompanied by permanent changes in the nervous system resulting in neurological deficits or neuropathy.

Article at a Glance:

Cocaine is a very potent stimulant of the nervous system 

Cocaine use affects multiple brain systems resulting in increased impulsiveness and risk-taking, decreased cognitive ability and increased sensitivity to stress and increased anxiety

Cocaine is comorbid with psychiatric and substance use disorders

Mood disorders may make individuals more susceptible to cocaine use

Cocaine Impacts the Brain Reward Pathway

Dopamine is a neurotransmitter that is involved in motivated behaviors and is part of the brain reward pathway which mediates the individual’s response to natural rewards (food, social interactions, sex, etc.). The pleasurable and euphoric feelings produced by cocaine are due to its effects on these reward pathways. Long-term cocaine use leads to dysregulation of the dopaminergic reward pathway. The dopaminergic reward pathway sends out projections to the frontal cortex. Changes in this pathway are responsible for impaired executive function and impulsiveness. Chronic cocaine use produces lasting changes in the reward pathway and such changes are considered to be responsible for drug dependence and relapse. 

Although the dopaminergic system is the most studied in association with cocaine addiction, chronic cocaine use also results in changes in other neurotransmitter systems, including serotonin, norepinephrine and endogenous opioids like endorphins.

Cocaine Influences Stress and Anxiety Circuits

Although a considerable amount of work has focused on the changes in the reward pathway that is responsible for the reinforcement of drug intake, the stress system also plays an important role during abstinence from cocaine use. Abstinence from drug use results in the activation of the stress axis, accompanied by increased irritability, depression, anxiety and an inability to feel pleasure. The stress system is considered to play an important role in the relapse to substance use, especially given the severe depressive symptoms experienced during times of withdrawal. Chronic cocaine use may result in changes in responsivity of the stress axis. 

Cocaine Influences the Volume of White and Gray Matter

Chronic cocaine use is associated with altered activation patterns in forebrain regions like the orbitofrontal cortex, the anterior cingulate cortex and the prefrontal cortex. These regions are responsible for cognitive functions like decision making and inhibiting impulsive behaviors. 

Changes in these areas due to cocaine use are substantiated by evidence of damage to both white and gray matter in these brain regions. Gray matter is composed of the cell bodies of neurons. Gray matter volume is connected with the structural and functional integrity of brain regions. Long-term cocaine use is associated with a decline in gray matter in the frontal and temporal cortices. These regions are associated with visual and verbal memory, executive functions like decision making and attention span. 

White matter in the brain mostly consists of axons. The integrity of white matter suggests connectivity between brain regions. White matter tracts that relay information between the frontal lobes of the brain show reduced integrity in long-term cocaine users. Such a decline in connectivity between the frontal lobes is associated with impulsiveness. Chronic cocaine use is also associated with motor deficits that are accompanied by a decline in gray and white matter in the cerebellum.

Cocaine Increases Cerebrovascular Constriction

Cocaine intake results in an increase in the release of catecholamines (epinephrine). The increased levels of catecholamines, in turn, result in the constriction of arterial blood vessels, including cerebral blood vessels. Chronic cocaine use results in deficits in brain perfusion (delivery of blood to an organ) in the frontal and temporal cortices and thus, may be partially responsible for the cognitive deficits seen in cocaine users. Cocaine can also cause various cardiovascular complications that may result in brain hemorrhages and infarctions. 

Cocaine Use is Comorbid With Other Mood Disorders

Cocaine addiction is often comorbid with other psychiatric disorders such as depressionanti-social personality disorder (ASPD), attention deficit disorder (ADD), anxiety disordersphobias and other substance use disorders. Chronic cocaine use can cause depression and alcohol abuse and worsen the symptoms of other disorders. However, cocaine use may be a coping mechanism for other mood disorders, with ASPD, anxiety disorders and ADD often preceding cocaine addiction.

If you or a loved one live with a cocaine addiction, contact The Recovery Village today to speak with a representative about how addiction treatment can help. The Recovery Village focuses on not only treating the addiction but also addressing any co-occurring mental health disorders, providing each patient with the personalized care they deserve. Take the first step toward a healthier future by calling today.

Thomas Christiansen
Editor – Thomas Christiansen
With over a decade of content experience, Tom produces and edits research articles, news and blog posts produced for Advanced Recovery Systems. Read more
Deep Shukla
Medically Reviewed By – Dr. Deep Shukla, PhD, MS
Dr. Deep Shukla graduated with a PhD in Neuroscience from Georgia State University in December 2018. Read more
Sources

Nestler EJ. “The neurobiology of cocaine addiction.” Science & Practice Perspectives, December 2005. Accessed May 22, 2019.

Weiss F., Koob GF. “Drug addiction: functional neurotoxicity of the brain reward systems.” Neurotoxicity Research, January 2001. Accessed May 22, 2019.

Goeders NE. “The HPA axis and cocaine reinforcement.” Psychoneuroendocrinology, January 2002. Accessed May 22, 2019.

Moeller FG., Hasan KM., Steinberg JL., Kramer LA., Dougherty DM., Santos RM., Valdes I., Swann AC., Barratt ES., Narayana PA. “Reduced anterior corpus callosum white matter integrity is related to increased impulsivity and reduced discriminability in cocaine-dependent subjects: diffusion tensor imaging.” Neuropsychopharmacology, March 2005. Accessed May 22, 2019.

Sim ME., Lyoo IK., Streeter CC., Covell J., Sarid-Segal O., Ciraulo DA., Kim MJ., Kaufman MJ., Yurgelun-Todd DA., Renshaw PF. “Cerebellar gray matter volume correlates with duration of cocaine use in cocaine-dependent subjects.” Neuropsychopharmacology, October 2007. Accessed May 22, 2019.

Ernst T., Chang L., Oropilla G., Gustavson A., Speck O. “Cerebral perfusion abnormalities in abstinent cocaine abusers: a perfusion MRI and SPECT study.” Psychiatry Research: Neuroimaging, August 2000. Accessed May 22, 2019.

Medical Disclaimer

The Recovery Village aims to improve the quality of life for people struggling with substance use or mental health disorder with fact-based content about the nature of behavioral health conditions, treatment options and their related outcomes. We publish material that is researched, cited, edited and reviewed by licensed medical professionals. The information we provide is not intended to be a substitute for professional medical advice, diagnosis or treatment. It should not be used in place of the advice of your physician or other qualified healthcare providers.