Nonatherosclerotic Vasculopathies

Caplan, Louis R.

doi:10.1016/b978-1-4160-4721-6.50013-4

Cited by 4 publications

(2 citation statements)

References 528 publications

(588 reference statements)

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“…While some cerebral ischaemic symptoms are a result of poor poststenotic perfusion, most are secondary to embolic events 7 21 31. Therefore, management of ICA dissection focuses on minimising these events through anticoagulant or antiplatelet treatment for at least 3 months postdissection 32. Swift implementation of therapy reduces the likelihood of embolic events originating from the dissection.…”

Section: Discussionmentioning

confidence: 99%

Rare case of bilateral traumatic internal carotid artery dissection

et al. 2016

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A 55-year-old man was working in a trench when the wall collapsed in on him, pinning him to the wall. On arrival in the emergency department the patient began reporting of right-sided headache. Neurological examination revealed left-sided reduced sensation with weakness. Whole-body CT scan showed right-sided flail chest and bilateral haemothorax as well as loss of flow and thinning of the distal right internal carotid artery (ICA) and loss of grey white matter differentiation in keeping with traumatic ICA dissection with a right middle cerebral artery (MCA) infarct. He was started on aspirin 300 mg once daily. 3 days postadmission the patient experienced worsening of vision and expressive dysphasia. CT angiogram showed bilateral ICA dissections extending from C2 to the skull base. The patient was managed conservatively in the stroke unit for infarction and was discharged home for follow-up in stroke clinic.

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Section: Discussionmentioning

confidence: 99%

Rare case of bilateral traumatic internal carotid artery dissection

et al. 2016

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“…Ca 2+ can freely pass through the cell membrane upon NMDAR activation, resulting in an increase of intracellular Ca 2+ levels (Newcomer et al 2000). Furthermore, during ischemia, K extracellular space due to ATP deficiency, whereas intracellular calcium efflux is blocked (impaired plasma membrane-associated Ca 2+ /ATPase and Na /Ca 2+ exchanger), culminating in a dramatic increase in intracellular calcium concentration (Caplan and Biller 2000). Additionally, excess Ca 2+ activates calpain in postsynaptic neurons via NMDAR, inhibiting Na /Ca 2+ X3…”

Section: Pathology Of Ischemic Strokementioning

confidence: 99%