Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Occlusion of the rodent middle cerebral artery by embolism, using an intraluminal filament, produces behavioral alterations which resemble many symptoms associated with stroke. This model has been used to examine treatment interventions for the disease, however, variable success rate in completely blocking the middle cerebral artery may present inconclusive interpretation of the data. To detect successful occlusion of the middle cerebral artery, we demonstrate here sensitive and reliable behavioral parameters including the elevated body swing test, the postural tail-hang test, the spontaneous rotational test, and the forelimb akinesia test. These assays provide a criterion for identifying animals with incomplete occlusion which could promote host-related spontaneous recovery and might confound true effects of experimental therapies on ischemia-induced dysfunctions. From a practical standpoint, the early reliable identification of partial cerebral ischemia aids in immediate and efficient adjustments of the surgical procedure to create a complete and stable ischemia stroke animal model.
 ...
PMID:Early assessment of motor dysfunctions aids in successful occlusion of the middle cerebral artery. 985 69

Rodents have been extensively used for experimental stroke research with rat and gerbil the preferred species. With the advent of transgenesis and gene targeting the number of mutant mouse strains is rapidly increasing. Thus, mouse models of stroke will be of great importance in the analysis of genetic factors affecting stroke. Demonstrating long-term functional recovery is of paramount importance for the pharmacological evaluation of putative stroke therapies. In the present paper we induce mild focal cerebral ischemia by tandem occlusion of the right middle cerebral artery (MCA), via craniotomy, together with the common carotid artery for 45 min in C57BL/6 strain of mice. The effects of ischemia were evaluated acutely by MRI and long-term (> 3 weeks) sensorimotor functional deficits were analyzed using a number of behavioral paradigms including the rotorod, wire hang, horizontal surface approach, eye-closure reflex, and T-maze tests. Although the induced brain damage is mild we show that it leads to clearly detectable and significant sensorimotor defects associated with fine motor coordination, balance, and postural and sensory reflexes. We conclude that the applied behavioral tests will be useful in the analysis of stroke in mutant mice.
 ...
PMID:Transient focal cerebral ischemia induces sensorimotor deficits in mice. 1068 Jul 58

Carotid artery dissection followed by cerebral infarction as a result of blunt trauma can occur in a number of forensically relevant situations. We describe two such cases. In the first case, a 19-year-old female was involved in a road traffic accident, when her car crashed into the rear of another car. Initially, the young woman presented a minor head injury without loss of consciousness and minor bruising to the left side of the neck. After 48 h, she had developed confusion, speech difficulties, right facial nerve paralysis, and right hemiplegia. CT scan and carotid angiography showed cerebral ischemia with infarction in the territory of the middle left cerebral artery and complete dissection of the left carotid artery. In the second case, a 33-year-old male with depression attempted to hang himself. The rope gave way and he fell down. He had also taken a paracetamol, and a non-steroidal anti-inflammatory drug overdose. He did not lose consciousness but appeared withdrawn and depressed. Approximately 6 h later, his conscious state deteriorated. A CT scan revealed thrombosis of the left internal carotid artery, extending to the middle cerebral artery. The patient died. Both cases reinforce the need for full neurological assessment and review of any individual subject to blunt trauma to the neck, whether accidental or deliberate or where the history is incomplete. In the forensic setting, in particular, RTAs, suspension by the neck, strangulation, and garotting are all instances when examination and assessment must be thorough--and clear advice given--in the absence of any immediate signs or symptoms--that any new symptoms or signs require immediate and thorough neurological investigation. There should be low threshold for prolonged neurological observation or further neurovascular investigations such as ultrasound, CT or MRI scan or angiography, to minimize the risk of developing potentially fatal or incapacitating sequelae.
 ...
PMID:Delayed presentation of carotid dissection, cerebral ischemia, and infarction following blunt trauma: two cases. 1527 48

Cardiovascular and neurologic surgeries often involve a temporary reduction in cerebral blood flow. In these conditions, as well as during cerebral ischemia and traumatic brain injury, the temporary loss of oxygen and glucose initiates a cascade of cellular events that culminate in neuronal death and damage. Understanding the mechanisms that contribute to neuronal death after hypoxia/ischemia is critically important for treatment of such brain injury. Here, we use a model of combined cerebral hypoxia/ischemia (H/I) to examine the role of protease-activated receptor-1 (PAR-1) in hypoxic/ischemic neuronal damage. Our data show that PAR-1-deficient mice have smaller lesion volumes than wild-type controls after 45 minutes of H/I. The results of the genetic block of PAR-1 were corroborated using a PAR-1 antagonist, which decreased infarct volume in wild-type C57Bl6 mice. Examination of cellular responses to H/I reveals that PAR-1 -/- animals have less cellular death and diminished glial fibrillary acidic protein expression. Additionally, PAR-1 -/- mice exhibit less motor behavior impairment in rotorod and inverted wire-hang tests. These data suggest that PAR-1 contributes to hypoxic/ischemic brain injury and are consistent with other studies that implicate serine proteases and their receptors in neuropathology after cerebral insults.
 ...
PMID:PAR-1 deficiency protects against neuronal damage and neurologic deficits after unilateral cerebral hypoxia/ischemia. 1535 17