Long-term Cocaine Abuse Research Articles

Cervical kyphoscoliosis due to substance abuse: a case series on introduction and neurosurgical treatment.

A prospective case series. To investigate the possible associations of multi-directional cervical kyphoscoliosis (CKS) with substance abuse and evaluate treatment outcomes. CKS is a rare medical situation without a well-established pathology. Still there are many obscurities in treatment paradigms and outcomes. To our knowledge, there is no published report on the association between CKS with addiction. Besides the novel report of such a rare etiology for CSK, the complexity of the neurosurgical treatment makes this report the first of its kind. In this series, we presented three patients with a history of crack cocaine addiction who suffered CKS due to prolonged hand-over-neck posture and treated all of them with a complex neurosurgical protocol. All cases were operated on and restored their normal spine alignment. Their long-term outcomes showed independent neurological status with no major surgical complications. Crack cocaine addiction might be associated with CKS in long-term cocaine abuse. A complex neurosurgical approach can achieve a sustainable clinical outcome.

Cocaine induces vascular smooth muscle cells proliferation via DRP1-mediated mitochondrial fission and PI3K/HIF-1α signaling

Long-term cocaine abuse is associated with cardiovascular and pulmonary vascular complications. The vascular toxicity of cocaine can lead to vascular remodeling characterized by excessive proliferation of vascular smooth muscle cells. Though hypoxia-inducible factor (HIF) signaling and mitochondrial fission have been suggested to play essential roles in the pathogenesis of hypoxia-induced vascular remodeling, pathogenetic mechanism for cocaine-related vascular remodeling remains to be elucidated. In this study, we explore the effect of cocaine on the proliferation of vascular smooth muscle cells by in vitro experiments. The findings indicated that the cocaine-induced vascular smooth muscle cell hyperproliferation is achieved by enhancing DRP1-mediated mitochondrial fission and activating PI3K/HIF-1α signaling. Current findings suggested that mitochondrial fission would play a pivotal role in cocaine-related vascular remodeling and would be helpful in understanding the vascular toxicity of cocaine.

1457 Cocaine-Induced Colonic Ischemia

INTRODUCTION: Cocaine use is associated with arterial vasoconstriction and enhanced thrombus formation. Rarely, these effects on the intestinal blood supply result in intestinal ischemia. Cocaine-induced ischemic colitis is a relatively poorly-defined variant of this phenomenon, but some studies suggest it may be associated with higher morbidity and mortality than other etiologies. Therefore, timing is critical in both diagnosis and initiating treatments to prevent poor outcomes. We present a case of a middle-aged patient who had an unusual presentation for ischemic colitis due to cocaine abuse. CASE DESCRIPTION/METHODS: A 49-year-old male with a history remarkable only for alcohol and cocaine use disorders presented with a two day history of hematemesis with syncope and severe abdominal pain. Urine drug screen was positive for cocaine on admission, and initial workup with EGD was grossly unremarkable. An abdominal CT scan showed extensive circumferential submucosal fat but without colonic wall thickening or other signs of acute process, and a mesenteric angiography was similarly unrevealing. However, his clinical condition continued to deteriorate over the next 48 hours with worsening abdominal pain, and he began passing large melanic stools with occasional frank red blood. He subsequently became septic; due to concern for ischemic bowel, a colonoscopy was emergently performed. Diffuse severe ischemic changes with deep cratered ulcers in the descending, transverse, and ascending colon were noted. Emergent laparotomy was performed for a near-total colectomy, after which the patient began to stabilize. DISCUSSION: Long-term cocaine abuse is associated with multiple vascular morbidities, including bowel ischemia. Our patient presented in extremis due to bowel ischemia of both SMA and IMA territories requiring intensive care and emergent colectomy. Interestingly, despite the widespread vascular compromise, initial symptoms were nonspecific without blood per rectum and imaging was unremarkable, including CT and angiography. This illustrates the importance of maintaining clinical suspicion and the utility of colonoscopy in diagnosis, as his unusually diffuse disease eventually necessitated a colectomy in this middle-aged man with otherwise unremarkable medical history.

Acute Fibrinous and Organizing Pneumonia in a Long-term Cocaine Abuser

Acute Fibrinous and Organizing Pneumonia in a Long-term Cocaine Abuser

Cocaine Abusers Have an Overexpression of α-Synuclein in Dopamine Neurons

Alpha-synuclein is a presynaptic protein that has been implicated as a possible causative agent in the pathogenesis of Parkinson's disease. The native protein is a major component of nigral Lewy bodies in Parkinson's disease, and full-length alpha-synuclein accumulates in Lewy neurites. Here we present evidence that alpha-synuclein levels are elevated in midbrain dopamine (DA) neurons of chronic cocaine abusers. Western blot and immunoautoradiographic studies were conducted on postmortem neuropathological specimens from cocaine users and age-matched drug-free control subjects. The results demonstrated that alpha-synuclein levels in the DA cell groups of the substantia nigra/ventral tegmental complex were elevated threefold in chronic cocaine users compared with normal age-matched subjects. The increased protein levels in chronic cocaine users were accompanied by changes in the expression of alpha-synuclein mRNA in the substantia nigra and ventral tegmental area. Although alpha-synuclein expression is prominent in the hippocampus, there was no increase in protein expression in this brain region. The levels of beta-synuclein, a possible negative regulator of alpha-synuclein, also were not affected by cocaine exposure. Alpha-synuclein protein levels were increased in the ventral tegmental area, but not the substantia nigra, in victims of excited cocaine delirium who experienced paranoia, marked agitation, and hyperthermia before death. The overexpression of alpha-synuclein may occur as a protective response to changes in DA turnover and increased oxidative stress resulting from cocaine abuse. However, the accumulation of alpha-synuclein protein with long-term cocaine abuse may put addicts at increased risk for developing the motor abnormalities of Parkinson's disease.

Cocaine-Induced Erythrocytosis and Increase in von Willebrand Factor

Mechanisms that mediate cocaine-induced cardiovascular events following vasoconstriction are incompletely understood. To examine the effects of cocaine in moderate doses on hematologic and hemostatic parameters that influence blood viscosity and thrombotic potential. Changes in hemoglobin concentration, hematocrit, and red blood cell counts were measured in human subjects who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for long-term cocaine abuse, before and sequentially after moderate intranasal and intravenous doses of cocaine. Hemostatic parameters, including von Willebrand factor, fibrinolytic activity, fibrinogen, plasminogen activator inhibitor antigen, and tissue-type plasminogen activator antigen, were sequentially measured after intravenous cocaine or saline placebo with cardiac troponin subunits T and I. Hemoglobin level (P= .002), hematocrit (P =.01), and red blood cell counts (P = .04) significantly increased from 4% to 6% over baseline from 10 to 30 minutes after intranasal (n = 14) and intravenous (n = 7) cocaine administration in doses of 0.9 mg/kg and 0.4 mg/kg, respectively, with no change in white blood cell or platelet counts. There was a significant increase (P =.03) in von Willebrand factor from 30 to 240 minutes, peaking at 40% over baseline following intravenous cocaine administration in a dose of 0.4 mg/kg (n = 12), with no change after 0.2 mg/kg (n = 3) or placebo (n = 6). Other hemostatic factors, creatinine, blood urea nitrogen, and cardiac troponin subunits T and I showed no changes. Cocaine induced a transient erythrocytosis that may increase blood viscosity while maintaining tissue oxygenation during vasoconstriction. An increase in von Willebrand factor without a compensatory change in endogenous fibrinolysis may trigger platelet adhesion, aggregation, and intravascular thrombosis.

Parkinsonism Associated With Long-term Cocaine Abuse

Cocaine abuse may produce several medical complications.¹Reported neurologic complications include headache, seizures, focal neurologic defects due to ischemia and/or hemorrhage, subarachnoid hemorrhage, and exacerbation of the symptoms of Tourette syndrome.^1-3We describe a patient in whom parkinsonism developed in association with long-term cocaine abuse, a complication not previously reported, to our knowledge. <h3>Report of a Case.</h3> A 35-year-old man with a 20-year history of drug addiction had consumed amphetamine and cannabis until he was 20 years old. After that, he began using both intranasal and intravenous cocaine several days a week. He complained of having evolution tremors for 1 year. The tremors, which began in his right arm and later affected his left arm as well, made it impossible for him to do his job for the last 2 months before he came to the hospital. Physical examination revealed a loss of corporal mobility and facial expression.

Parkinsonism associated with long-term cocaine abuse

Parkinsonism associated with long-term cocaine abuse

Cocaine Addiction: Psychology and Neurophysiology

Cocaine was considered incapable of producing dependence in 1980 but was recently proclaimed the drug of greatest national health concern. Recent clinical and preclinical investigations demonstrate that cocaine produces unique abuse and withdrawal patterns that differ from those of other major abused drugs and suggest that long-term cocaine abuse produces neurophysiological alterations in specific systems in the central nervous system that regulate the capacity to experience pleasure. It will be necessary to develop clinically pertinent research models before these findings can be considered definitive, but these evolving ideas have already led to applications of promising experimental treatments for cocaine abuse.

Vascular Changes in the Nasal Submucosa of Chronic Cocaine Addicts

A detailed, correlative, histologic evaluation of postmortem changes in the nasal mucosa of chronic cocaine users has shown characteristic mucosal and arteriolar changes as well as typical perivascular and subepithelial alterations compatible with chronic inflammation. These findings confirm and extend recent reports on the effects of cocaine in the coronary circulation and heart muscle as well as provide a new diagnostic tool to the forensic pathologist who suspects that a decedent has been a long-term cocaine abuser.

Cerebral Vasculitis Associated With Cocaine Abuse or Subarachnoid Hemorrhage?

To the Editor. —I read with interest the recent article by Kaye and Fainstat.1I would like to describe a patient who developed white-matter disease apparently related to long-term cocaine abuse. To my knowledge, this hazard of cocaine abuse has not been reported previously. Report of a Case. —A 27-year-old man presented with a left-sided seizure. During the past few weeks, he had noticed heaviness and paresthesias in his lower extremities and periods of forgetfulness. His medical history was unremarkable except for occasional intranasal use of cocaine during the past five years. He denied intravenous drug or alcohol abuse and there was no history of cardiac or collagen vascular disease. Examination disclosed the following values: blood pressure, 110/60 mm Hg; pulse rate, 88 beats per minute; and respirations, 18/min. He was alert, oriented, and without focal neurological findings. Contrast-enhanced computed tomographic scans of the head were normal (Fig 1).