Carotid artery dissection due to elongated styloid process: a self-stabbing phenomenon.

Elongated styloid process (ESP) is an anatomical variant that has been described as the cause of Eagle syndrome. Until recently, the styloid process has not been appreciated as a significant contributor to carotid artery dissection (CAD), which is not part of Eagle syndrome. We present a case of a 41-year-old male who presented with acute right middle cerebral artery occlusion and was found to have ESP projecting to and abutting the lateral wall of a dissected right internal carotid artery (ICA). Forced sustained head turning with maximal muscle contraction was the initiating event driving the styloid process into the wall of the ICA in a manner that can be likened to being stabbed with a pointed object. Knowing the association between ESP, Eagle syndrome, and CAD shall lead to increased awareness and appropriate diagnosis and treatment.

Endovascular treatment of symptomatic intracranial atherosclerotic disease.

Symptomatic intracranial atherosclerotic disease (ICAD) is responsible for approximately 10% of all ischemic strokes in the United States. The risk of recurrent stroke may be as high as 35% in patient with critical stenosis >70% in diameter narrowing. Recent advances in medical and endovascular therapy have placed ICAD at the forefront of clinical stroke research to optimize the best medical and endovascular approach to treat this important underlying stroke etiology. Analysis of symptomatic ICAD studies lead to the question that whether angioplasty and/or stenting is a safe, suitable, and efficacious therapeutic strategy in patients with critical stenoses that are deemed refractory to medical management. Most of the currently available data in support of angioplasty and/or stenting in high risk patients with severe symptomatic ICAD is in the form of case series and randomized trial results of endovascular therapy versus medical treatment are awaited. This is a comprehensive review of the state of the art in the endovascular approach with angioplasty and/or stenting of symptomatic ICAD.

Thrombolytic therapy in a patient with acute ischemic stroke caused by aortic dissection.

The current medical literature indicates a poor outcome in patients with ischemic stroke in the presence of aortic dissection, especially in those who underwent thrombolytic therapy. We report a favorable outcome in a patient with acute stroke who received rt-PA and was later found to have Stanford type A aortic dissection.

Delayed olfactory nerve regeneration in ApoE-deficient mice.

Apolipoprotein E (apoE), a lipid transporting protein, is extensively expressed in the primary olfactory pathway, but its function is unknown. We previously reported increased apoE levels in the olfactory bulb (OB) following olfactory epithelium (OE) lesion in mice, and hypothesized that apoE may play a vital role in olfactory nerve (ON) regeneration. To directly test this hypothesis, we examined the rate of ON regeneration following OE lesion in apoE deficient/knockout (KO) and wild-type (WT) mice. OE was lesioned in 2- to 3-month-old mice by intranasal irrigation with Triton X-100 (TX). OB were collected at 0, 3, 7, 21, 42, and 56 days post-lesion. OB recovery was measured by both immunoblotting and immunohistochemical analysis of growth cone associated protein (GAP) 43 and olfactory marker protein (OMP). The results revealed that (1) OMP recovery in the OB was significantly slower in apoE KO compared to WT mice; (2) recovery of glomerular area was similarly slower; and (3) GAP43 increases and return to prelesion levels in the OB were slower in KO mice. Together, these results show that olfactory nerve regeneration is significantly slower in KO mice as compared to WT mice, suggesting apoE facilitates olfactory nerve regeneration.