scholarly journals Lasting Pure-Motor Deficits after Focal Posterior Internal Capsule White-Matter Infarcts in Rats

2015 ◽  
Vol 35 (6) ◽  
pp. 977-984 ◽  
Author(s):  
Francesco Blasi ◽  
Michael J Whalen ◽  
Cenk Ayata
Keyword(s):  
White Matter ◽  
Internal Capsule ◽  
Experimental Models ◽  
White Matter Injury ◽  
Motor Deficits ◽  
Sprague Dawley ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Endothelin 1 ◽  
Pure Motor

Small white-matter infarcts of the internal capsule are clinically prevalent but underrepresented among currently available animal models of ischemic stroke. In particular, the assessment of long-term outcome, a primary end point in clinical practice, has been challenging due to mild deficits and the rapid and often complete recovery in most experimental models. We, therefore, sought to develop a focal white-matter infarction model that can mimic the lasting neurologic deficits commonly observed in stroke patients. The potent vasoconstrictor endothelin-1 ( n = 24) or vehicle ( n = 9) was stereotactically injected into the internal capsule at one of three antero-posterior levels (1, 2, or 3 mm posterior to bregma) in male Sprague-Dawley rats. Endothelin-injected animals showed highly focal (~1 mm3) and reproducible ischemic infarcts, with severe axonal and myelin loss accompanied by cellular infiltration when examined 2 and 4 weeks after injection. Only those rats injected with endothelin-1 at the most posterior location developed robust and pure-motor deficits in adhesive removal, cylinder and foot-fault tests that persisted at 1 month, without detectable sensory impairments. In summary, we present an internal capsule stroke model optimized to produce lasting pure-motor deficits in rats that may be suitable to study neurologic recovery and rehabilitation after white-matter injury.

White Matter Injury in Premature Newborns

2016 ◽  
Vol 35 (2) ◽  
pp. 73-77 ◽  
Author(s):  
Dawn Gano
Keyword(s):  
Brain Injury ◽  
White Matter ◽  
White Matter Injury ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Premature Newborns ◽  
Preterm Newborns

AbstractPreterm newborns are highly susceptible to brain injury. White matter injury is among the dominant patterns of brain injury in preterm newborns. The purpose of this review is to discuss the pathogenesis, diagnosis, management, and prevention of white matter injury in premature newborns. The long-term outcome of white matter injury in children born prematurely is also addressed.

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 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.

scholarly journals Long-Term Outcome Following Decompressive Craniectomy in Pediatric Penetrating Blast Brain Injury; a Prospective Study

2021 ◽  
Vol 8 (4) ◽  
Author(s):  
Seyed Amir Hossein Javadi ◽  
Parisa Balu ◽  
Fereshteh Naderi Behdani ◽  
Amir Hossein Orandi ◽  
Ehsan Ahmadipour ◽  
...  
Keyword(s):  
Brain Injury ◽  
Decompressive Craniectomy ◽  
Early Death ◽  
Motor Deficits ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Number Of Patients ◽  
Secondary Injuries ◽  
A Prospective Study

Background: Brain penetrating blast injury is a leading cause of early death due to excessively elevated intracranial pressure (ICP), culminating in trans-tentorial herniation. The role of craniectomy to decrease ICP and secondary injuries has been controversial particularly in pediatric patients. Three cases of pediatric penetrating blast injuries undergoing decompressive craniectomy are reported in Methods: The current study was a prospective series, including fifteen cases of pediatric blast-related brain injury referred to the emergency ward during a period of two years. Three survived patients had a Glasgow Coma Scale (GCS) of four along with anisocoric pupillary light reflex (PLR). Decompressive craniectomy and ventriculostomy (EVD) were performed. The patients underwent ICP monitoring for two weeks. Results: Early postoperative GCS (5 days) was 7/15 in all three patients. Two weeks and one month’s GCS were 9 and 14, respectively. After three months, cranioplasty was performed. Long-term follow-up detected no major motor deficits after one year and was associated with excellent school performance. Neuroplasticity resulted in contralateral dominancy and handedness in one case. Conclusions: Survivors of pediatric blast brain injury had a favorable outcome after decompressive craniectomy in the current paper. However, there was a limited number of patients, and the results could not be generalized. Further research in this regard with larger sample size is recommended.

scholarly journals Modified behavioural tests to detect white matter injury- induced motor deficits after intracerebral haemorrhage in mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Weixiang Chen ◽  
Min Xia ◽  
Chao Guo ◽  
Zhengcai Jia ◽  
Jie Wang ◽  
...  
Keyword(s):  
White Matter ◽  
Grip Strength ◽  
Motor Function ◽  
Intracerebral Haemorrhage ◽  
Strength Test ◽  
White Matter Injury ◽  
Motor Deficit ◽  
Motor Deficits ◽  
Walking Test ◽  
Behavioural Tests

AbstractMotor function deficit induced by white matter injury (WMI) is one of the most severe complications of intracerebral haemorrhage (ICH). The degree of WMI is closely related to the prognosis of patients after ICH. However, the current behavioural assessment of motor function used in the ICH mouse model is mainly based on that for ischaemic stroke and lacks the behavioural methods that accurately respond to WMI. Here, a series of easy-to-implement behavioural tests were performed to detect motor deficits in mice after ICH. The results showed that the grip strength test and the modified pole test not only can better distinguish the degree of motor dysfunction between different volumes of blood ICH models than the Basso Mouse Scale and the beam walking test but can also accurately reflect the severity of WMI characterized by demyelination, axonal swelling and the latency of motor-evoked potential delay induced by ICH. In addition, after ICH, the results of grip tests and modified pole tests, rather than the Basso Mouse Scale and the beam walking test, were worse than those observed after intraventricular haemorrhage (IVH), which was used as a model of brain haemorrhage in non-white matter areas. These results indicate that the grip strength test and the modified pole test have advantages in detecting the degree of motor deficit induced by white matter injury after ICH in mice.

scholarly journals The Potential of Stem Cell Therapy to Repair White Matter Injury in Preterm Infants: Lessons Learned From Experimental Models

2019 ◽  
Vol 10 ◽  
Author(s):  
Josine E. G. Vaes ◽  
Marit A. Vink ◽  
Caroline G. M. de Theije ◽  
Freek E. Hoebeek ◽  
Manon J. N. L. Benders ◽  
...  
Keyword(s):  
Stem Cell ◽  
White Matter ◽  
Cell Therapy ◽  
Preterm Infants ◽  
Stem Cell Therapy ◽  
Experimental Models ◽  
Lessons Learned ◽  
White Matter Injury

scholarly journals Synaptic Injury in the Thalamus Accompanies White Matter Injury in Hypoxia/Ischemia-Mediated Brain Injury in Neonatal Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Na Liu ◽  
Xin Tong ◽  
Wanjie Huang ◽  
Jianhua Fu ◽  
Xindong Xue
Keyword(s):  
White Matter ◽  
White Matter Injury ◽  
Neonatal Rat ◽  
Morris Water Maze Test ◽  
Neonatal Rats ◽  
Sprague Dawley ◽  
Artery Ligation ◽  
Compensatory Response ◽  
Significant Difference ◽  
Hypoxia Ischemia

The broad spectrum of disabilities caused by white matter injury (WMI) cannot be explained simply by hypomyelination. Synaptic injury in the thalamus may be related to disabilities in WMI survivors. Neuronal injury in the thalamus has been found most commonly in autopsy cases of preterm WMI. We hypothesized that hypoxia/ischemia (HI) in neonatal rats results in synaptic abnormalities in the thalamus that contribute to disabilities in WMI survivors. We examined changes in synapses in a neonatal rat model of HI-induced WMI. Right common carotid artery ligation and hypoxia (8% oxygen for 2.5 hours (h)) were performed in three-day-old Sprague-Dawley rats. We found HI rats performed worse in the Morris water maze test than sham rats, suggesting long-term cognition impairment after HI injury. A loss of synapses in the thalamus accompanied by hypomyelination and oligodendrocytes (OLs) reduction was observed. At the ultrastructural level, reductions in active zone (AZ) length and postsynaptic density (PSD) thickness were detected at 2 weeks after HI exposure. Furthermore, increased expression of synaptophysin and PSD-95 in both groups was observed from 3 days (d) to 21 d after hypoxic/ischemic (HI) injury. PSD-95 expression was significantly lower in HI rats than in sham rats from 14 d to 21 d after HI injury, and synaptophysin expression was significantly lower in HI rats from 7 d to 14 d after HI injury. However, no significant difference in synaptophysin expression was observed between HI rats and sham rats at 21 d after HI injury. The results demonstrated synaptic abnormalities in the thalamus accompanied by hypomyelination in WMI in response to HI exposure, which may contribute to the diverse neurological defects observed in WMI patients. Although synaptic reorganization occurred as a compensatory response to HI injury, the impairments in synaptic transmission were not reversed.

Effectiveness of minocycline in acute white matter injury after intracerebral hemorrhage

2016 ◽  
Vol 126 (6) ◽  
pp. 1855-1862 ◽  
Author(s):  
Xiang Zou ◽  
Zehan Wu ◽  
Wei Zhu ◽  
Liang Chen ◽  
Ying Mao ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Autologous Blood ◽  
Critical Role ◽  
White Matter Injury ◽  
High Morbidity ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Injection Group ◽  
Jnk Activation

OBJECTIVEIntracerebral hemorrhage (ICH) is a fatal disease with high morbidity and mortality, which may be followed by white matter injury (WMI) due to the local oxidizing reaction induced by iron (Fe). In this study, the authors examined the effect of the tetracycline antibiotic minocycline on Fe-induced WMI and c-Jun N-terminal kinase (JNK) activation in rats.METHODSThirty-six male Sprague-Dawley rats underwent an intracaudate injection of saline, Fe, or Fe + minocycline. Another 36 rats had an intracaudate injection of autologous blood and were treated with minocycline or vehicle (saline). Biomarkers of both WMI and JNK activation were examined.RESULTSIn the Fe-injection group, minocycline suppressed WMI labeled by β-amyloid precursor protein (β-APP) and degraded myelin basic protein (dMBP)/MBP ratio. Protein levels of phosphorylated-JNK were increased after Fe injection, and could be suppressed by minocycline treatment. In the autologous blood–injection group, β-APP and dMBP/MBP levels increased in the ipsilateral site compared with the contralateral site, which could be suppressed by 7 days of minocycline intervention.CONCLUSIONSIron plays a critical role in WMI after ICH, which can be suppressed by minocycline through reducing the damage induced by Fe.

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