scholarly journals Diffuse subcortical white matter injury and bilateral basal ganglia neuronal loss after acute opioid overdose

2020 ◽  
Vol 33 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Andreea I Dinicu ◽  
Amit Chaudhari ◽  
Simon Kayyal
Keyword(s):  
White Matter ◽  
Basal Ganglia ◽  
Neuronal Loss ◽  
Subcortical White Matter ◽  
White Matter Injury ◽  
Adolescent Male ◽  
Opioid Overdose ◽  
Diffuse White Matter ◽  
Neurological Exam ◽  
Life Threatening

Opiate intoxication has been associated with life-threatening effects of sympathetic suppression and respiratory depression, but current literature is limited in describing its neurotoxic effects on the central nervous system. Here, we present the case of an otherwise high-functioning adolescent male who was found unresponsive after ingestion of approximately 3–4 fake oxycodone 10–325 mg pills laced with fentanyl. Magnetic resonance imaging showed evidence of diffuse T2 hyperintensities in the corpus callosum and bilateral frontal, parietal, and cerebellum indicative of diffuse white matter injury. In addition, there were distinct areas of restricted diffusion in the bilateral basal ganglia concerning for oxidative stress-mediated neuronal loss. His neurological exam improved with supportive treatment over the course of his hospitalization. Although limited literature has shown leukoencephalopathy to be associated with opioid overdose, we present a case of additional involvement of subcortical gray matter.

A Girl of Unusual Diffuse White Matter and Basal Ganglia Lesions Following Streptococcus Pneumoniae Meningoencephalitis

2016 ◽  
Vol 24 (4) ◽  
pp. 266-271
Author(s):  
이훈상 ◽  
이윤진 ◽  
김영미 ◽  
Yeon Gyu Min ◽  
김경민 ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
White Matter ◽  
Basal Ganglia ◽  
Diffuse White Matter

scholarly journals Glutamate receptors: the cause or cure in perinatal white matter injury?

2010 ◽  
Vol 6 (4) ◽  
pp. 209-211 ◽  
Author(s):  
R. Douglas Fields
Keyword(s):  
White Matter ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Experimental Studies ◽  
Perinatal Period ◽  
White Matter Injury ◽  
Glutamate Toxicity ◽  
Diffuse White Matter ◽  
Group I

Glutamate toxicity from hypoxia-ischaemia during the perinatal period causes white matter injury that can result in long-term motor and intellectual disability. Blocking ionotropic glutamate receptors (GluRs) has been shown to inhibit oligodendrocyte injury in vitro, but GluR antagonists have not yet proven helpful in clinical studies. The opposite approach of activating GluRs on developing oligodendrocytes shows promise in experimental studies on rodents as reported by Jartzie et al., in this issue. Group I metabotropic glutamate receptors (mGluRs) are expressed transiently on developing oligodendrocytes in humans during the perinatal period, and the blood–brain-barrier permeable agonist of group I mGluRs, 1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD), reduces white matter damage significantly in a rat model of perinatal hypoxia-ischaemia. The results suggest drugs activating this class of GluRs could provide a new therapeutic approach for preventing cerebral palsy and other neurological consequences of diffuse white matter injury in premature infants.

scholarly journals Combining Hypothermia and Oleuropein Subacutely Protects Subcortical White Matter in a Swine Model of Neonatal Hypoxic-Ischemic Encephalopathy

2020 ◽  
Author(s):  
Jennifer K Lee ◽  
Polan T Santos ◽  
May W Chen ◽  
Caitlin E O’Brien ◽  
Ewa Kulikowicz ◽  
...  
Keyword(s):  
White Matter ◽  
Motor Cortex ◽  
Corpus Callosum ◽  
Internal Capsule ◽  
Subcortical White Matter ◽  
White Matter Injury ◽  
Swine Model ◽  
Cortex Neuron ◽  
Motor Cortex Neuron ◽  
Ischemic Encephalopathy

Abstract Neonatal hypoxia-ischemia (HI) causes white matter injury that is not fully prevented by therapeutic hypothermia. Adjuvant treatments are needed. We compared myelination in different piglet white matter regions. We then tested whether oleuropein (OLE) improves neuroprotection in 2- to 4-day-old piglets randomized to undergo HI or sham procedure and OLE or vehicle administration beginning at 15 minutes. All groups received overnight hypothermia and rewarming. Injury in the subcortical white matter, corpus callosum, internal capsule, putamen, and motor cortex gray matter was assessed 1 day later. At baseline, piglets had greater subcortical myelination than in corpus callosum. Hypothermic HI piglets had scant injury in putamen and cerebral cortex. However, hypothermia alone did not prevent the loss of subcortical myelinating oligodendrocytes or the reduction in subcortical myelin density after HI. Combining OLE with hypothermia improved post-HI subcortical white matter protection by preserving myelinating oligodendrocytes, myelin density, and oligodendrocyte markers. Corpus callosum and internal capsule showed little HI injury after hypothermia, and OLE accordingly had minimal effect. OLE did not affect putamen or motor cortex neuron counts. Thus, OLE combined with hypothermia protected subcortical white matter after HI. As an adjuvant to hypothermia, OLE may subacutely improve regional white matter protection after HI.

scholarly journals Risk Factors for Silent Cerebral Infarcts in Subcortical White Matter and Basal Ganglia

Stroke ◽  
1999 ◽  
Vol 30 (2) ◽  
pp. 378-382 ◽  
Author(s):  
Toshiyuki Uehara ◽  
Masayasu Tabuchi ◽  
Etsuro Mori
Keyword(s):  
Risk Factors ◽  
White Matter ◽  
Basal Ganglia ◽  
Subcortical White Matter ◽  
Cerebral Infarcts

MR Imaging and Proton MR Spectroscopy of the Brain in Behçet's Disease

2003 ◽  
Vol 16 (2) ◽  
pp. 267-273 ◽  
Author(s):  
M. Cellerini ◽  
M. Bartolucci ◽  
M. Mortilla ◽  
M. Mascalchi ◽  
F. Li Gobbi ◽  
...  
Keyword(s):  
White Matter ◽  
Basal Ganglia ◽  
Mr Imaging ◽  
Mr Spectroscopy ◽  
Subcortical White Matter ◽  
Neurological Involvement ◽  
Medium Size ◽  
Proton Mr Spectroscopy ◽  
Group A ◽  
Group B

Cerebral MR imaging (MR) and proton-MR spectroscopy (H-MRS) data are lacking in neurologically asymptomatic patients with Behçet's disease (BD). Aim of the following work was to assess MR and H-MRS characteristics of brain involvement over time in patients with BD without clinical neurological involvement. Forty cerebral MR and 12 H-MRS examinations obtained over a one to nine year follow-up in 17 patients with (group A n=9) or without (group B n=8) neurological involvement were retrospectively reviewed. Four group-B patients had a normal first MR examination whereas all group-A and four group-B patients showed single (n?3) or multiple (n=10) subcortical white matter foci of signal change. Large midbrain, basal ganglia or subcortical white matter lesions were depicted in six group-A patients. Comparison between initial and last MR examinations revealed 28 new small-to-medium size lesions. Over the course of the study, lesion enhancement was seen in five patients all belonging to group A. NAA/Cr and Cho/Cr ratios of supraventricular white matter did not show significant differences between patients and healthy controls or between group-A and group-B patients. Clinically silent cerebral involvement in the form of small-to-medium size subcortical lesions may be present at MR examination in BD patients. Large brainstem and basal ganglia lesions associated with overt neurological symptoms are characteristic of the disease. H-MRS of cerebral normal-appearing white matter does not show any significant metabolic change in BD.

scholarly journals Jaw Dystonia and Reversible Basal Ganglia Changes as an Initial Presentation of Systemic Lupus Erythematosus

2017 ◽  
Vol 8 (1) ◽  
pp. 31-34 ◽  
Author(s):  
Meghan Romba ◽  
Yujie Wang ◽  
Shu-Ching Hu ◽  
Sandeep Khot
Keyword(s):  
Systemic Lupus Erythematosus ◽  
White Matter ◽  
Basal Ganglia ◽  
Brain Imaging ◽  
Lupus Erythematosus ◽  
Subcortical White Matter ◽  
High Dose ◽  
Neuropsychiatric Lupus ◽  
Systemic Lupus ◽  
Traditional Treatment

Dystonia as a manifestation of neuropsychiatric lupus erythematosus (NPSLE) is uncommon. We report a 25-year-old woman who experienced progressive confusion, reduced speech, and difficulty opening her mouth approximately 2 weeks after development of a facial rash. Brain imaging showed bilateral, symmetric signal abnormalities within the basal ganglia and subcortical white matter. Despite treatment with high-dose steroids, she continued to have difficulty speaking with evidence of jaw dystonia on examination. Jaw dystonia rapidly improved with the initiation of levodopa. Repeat evaluation 3 months later exhibited the absence of jaw dystonia and near resolution of the imaging abnormalities. Our patient demonstrated a unique presentation with jaw dystonia refractory to traditional treatment for NPSLE. Such a presentation likely represents a severe variant of NPSLE requiring both immunosuppressive and symptomatic therapies.

scholarly journals Hemiballism-hemichorea Induced by Subcortical Ischemia

1993 ◽  
Vol 20 (4) ◽  
pp. 324-328 ◽  
Author(s):  
Fukhi Toshiya ◽  
Hasegawa YuKihiro ◽  
Seriyama Shinya ◽  
Takeuchi Toru ◽  
Sugita Koujiro ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Basal Ganglia ◽  
Subthalamic Nucleus ◽  
Clinical Manifestation ◽  
Cerebral Hemisphere ◽  
Subcortical White Matter ◽  
Pathological Changes ◽  
Limb Weakness ◽  
Involuntary Movements

ABSTRACT:Four patients presented with hemiballism-hemichorea as a clinical manifestation of white matter ischemia. These patients illustrate “positive” motor phenomena rather than limb weakness as a consequence of cerebral ischemia. In each patient, the involuntary movements disappeared following worsening of paresis. Subcortical white matter infarction in three patients and hemodynamic hypo-perfusion in the cerebral hemisphere contralateral to dyskinetic movements were possible causes. Neuroradiologically, none had pathological changes in the vicinity of the subthalamic nucleus. We presume from these observations that ischemia of the subcortical white matter, without involvement of the basal ganglia or the subthalamic nucleus, may cause hemiballism-hemichorea

scholarly journals Neurobehavioral Aspects of the Delayed Encephalopathy of Carbon Monoxide Intoxication: Case Report and Review

1995 ◽  
Vol 8 (1) ◽  
pp. 47-52 ◽  
Author(s):  
M. F. Mendez ◽  
R. C. Doss
Keyword(s):  
Carbon Monoxide ◽  
White Matter ◽  
White Matter Lesions ◽  
Subcortical White Matter ◽  
Clinical Aspects ◽  
Co Poisoning ◽  
Diffuse White Matter ◽  
Co Intoxication ◽  
Frontal Lobe Syndrome ◽  
Delayed Encephalopathy

We report the neurobehavioral aspects of the delayed encephalopathy of carbon monoxide (CO) intoxication in a 29 year old woman and review the literature. Four weeks after CO poisoning, the patient developed a frontal lobe syndrome, visuoperceptual impairment, and diffuse white matter lesions with an otherwise normal neurological examination. In contrast, patients with the classical syndrome also have a parkinsonian state or an akinetic–mute state. The delayed encephalopathy of CO poisoning usually results from demyelination of subcortical white matter, necrosis of the globus pallidus, or both. The clinical aspects, risk factors, neurobiological features, and therapy and prognosis are discussed.

scholarly journals Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury

2015 ◽  
Vol 36 (1) ◽  
pp. 187-198 ◽  
Author(s):  
Akihiro Shindo ◽  
Anna C Liang ◽  
Takakuni Maki ◽  
Nobukazu Miyamoto ◽  
Hidekazu Tomimoto ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Ischemia ◽  
Nerve Conduction ◽  
Neurovascular Unit ◽  
Cell Types ◽  
Subcortical White Matter ◽  
Experimental Models ◽  
White Matter Injury ◽  
Cerebral White Matter ◽  
Myelin Sheaths

Oligodendrocytes are one of the major cell types in cerebral white matter. Under normal conditions, they form myelin sheaths that encircle axons to support fast nerve conduction. Under conditions of cerebral ischemia, oligodendrocytes tend to die, resulting in white-matter dysfunction. Repair of white matter involves the ability of oligodendrocyte precursors to proliferate and mature. However, replacement of lost oligodendrocytes may not be the only mechanism for white-matter recovery. Emerging data now suggest that coordinated signaling between neural, glial, and vascular cells in the entire neurovascular unit may be required. In this mini-review, we discuss how oligodendrocyte lineage cells participate in signaling and crosstalk with other cell types to underlie function and recovery in various experimental models of subcortical white-matter injury.

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