With paired t-tests, DPA-714 volume of distribution lesioned and normal appearing white matter (NAWM) were compared within subjects, to investigate inflammation. Total and regional (juxtacortical, periventricular, deep white matter and infratentorial) lesion burden were compared between the groups with one-way ANOVA. In this exploratory study, 15 chemotherapy-treated and 15 age-matched chemotherapy-naïve patients with early-stage breast cancer, as well as 15 healthy controls underwent simultaneous PET-MR neuroimaging, including T1-weighted MPRAGE, T2-weighted FLAIR and dynamic PET with the 18-kDA translocator protein (TSPO) radioligand DPA-714. Therefore, we investigated the presence of leukoencephalopathy after multiagent chemotherapy in women treated for breast cancer and potential underlying neuroinflammatory processes. This case demonstrated a rare and significant complication of heroin inhalation: HIL and rTTC and described potential therapies currently being studied.Īlthough chemotherapy-induced leukoencephalopathy has been described in case and cohort studies, literature remains inconclusive about its prevalence and mechanisms. The patient's symptoms were treated as currently there is no guideline directed therapy for HIL or rTTC. Transesophageal echocardiogram demonstrated a classic basal hypokinesis and ballooning characteristic of rTTC. Medical course was complicated by a rare associated feature of HIL: reverse Takotsubo cardiomyopathy (rTTC). Symptoms progressively worsened over the course of multiple weeks and brain imaging was consistent with toxic leukoencephalopathy secondary to heroin inhalation. This case highlights a patient with a history of heroin inhalation who presented with multiple neurological features, including bilateral upper and lower extremity weakness, blurry vision and slurred speech.

Since then, there have been many documented cases of heroin-induced leukoencephalopathy (HIL) and takotsubo cardiomyopathy (TTC). The practice of heating heroin and inhaling its vapors, commonly referred to as “chasing the dragon” has been around for decades, but only gained popularity in the United States in the 1990s. These four cases, with their varied presenting symptoms, clinical courses, and degree of pathology, emphasize the importance of considering toxic leukoencephalopathy as an etiology of acute neurologic deterioration following high-dose chemotherapy. The location and extent of the central nervous system pathology correlated with the type and severity of clinical symptoms. The white matter was affected by severe myelin pallor, edema, and a prominent macrophage infiltrate in each of the cases. The neuropathologic findings in these cases, although similar, varied in severity and distribution. The fourth was a 49-year-old female patient who was treated with multiple chemotherapeutics for Stage II breast carcinoma and subsequently developed visual acuity and field defects. The third was a 16-year-old male who developed a profound peripheral and central neuropathy after chemotherapy treatment for T-cell acute lymphoblastic leukemia. The second was a 36-year-old male who developed mental status changes, ataxia and dysarthria following treatment for lymphoma. He presented with confusion and focal seizures with a rapid progression to coma and decerebrate posturing. The first was a 56-year-old male treated with multiple chemotherapeutics for multiple myeloma. We report here three patients with hematologic malignancies and one patient with metastatic carcinoma with chemotherapy-induced leukoencephalopathy. The brain and spinal cord were examined routinely, and histological sections were taken for evaluation. Autopsies of four cases of toxic leukoencephalopathy were performed following standard protocols. One complication is toxic leukoencephalopathy, which is due to a direct toxic effect of chemotherapeutic agents on the central nervous system white matter. We have observed an increasing number of autopsies on patients with chemotherapy-related complications.

Taxol taxic levels in thebrain