[A case of a traumatic anterior cerebral artery aneurysm following the penetration of the skull base by an iron rod].

A 61-year-old male fell from a position 1 m high when building a house. An iron rod, which protruded upward from a solid base in cement, penetrated this patient's neck 15 cm to the head and was successfully extracted by himself. On admission, he complained of headache and vomiting. General examination disclosed nasal bleeding, intraoral bleeding, and L figured skin laceration in the left side of his neck at the level of the thyroid cartilage. Mild disorientation (JCS2) was noted. Otolaryngological examination disclosed hyperemia on the left side of the vocal cord as well as at the dome of the superior pharynx. Plain skull film disclosed pneumocephalus and that a piece of bone fragment of the planum sphenoidale had penetrated the brain. CT demonstrated air in the subarachnoid space, ventricular hemorrhage, intracerebral hematoma in the right frontal lobe, and subarachnoid hemorrhage in the anterior interhemispheric fissure. CAG detected neither cerebral vascular abnormalities nor cerebral aneurysm. While staying in our department, he developed mild fever and CSF rhinorrhea. The diagnosis of bacterial meningitis was made from the CSF finding and was well controlled with conservative therapy. CSF rhinorrhea stopped spontaneously with conservative treatment. Sagittal MRI continuously demonstrated contusional hematoma in the base of the right frontal lobe just above the fractured planum sphenoidale and genu of the corpus callosum following the course of the intracranially invading iron rod. The right CAG on Day 10 demonstrated vasospasm on the A1 and a 1 cm sized saccular cerebral aneurysm at the proximal right fronto-polar artery. CAG on Day 17 again showed the persistent presence of the aneurysm. For the purpose of preventing delayed rupture of the aneurysm, radical surgical treatment was planned. Microsurgical dissection disclosed that the aneurysm was located just behind the elevated fracture of the planum sphenoidale. Severe arachnoid adhesion was noted around the aneurysm. The aneurysm was successfully clipped with preservation of the parent artery without inducing new neurological deficits. From the general, otolaryngological, neuroradiological, and operative findings, this aneurysm was diagnosed as a traumatic cerebral artery aneurysm following the penetration of the skull base by the iron rod. The CAG performed at 8 months postoperatively demonstrated the patency of the parent artery and that there was no recurrence of the aneurysm. An unusual case of a traumatic cerebral artery aneurysm following the penetration of the skull base by an iron rod was thus reported.

Existence of c-kit receptor-positive, tryptase-negative, IgE-negative cells in human allergic nasal mucosa: a candidate for mast cell progenitor.

The accumulation of mast cells in the allergic nasal epithelium is well known, yet the mechanism remains unclear. We studied whether there is a candidate for mast cell progenitors in the allergic nasal mucosa tissue removed at the time of surgery. We first confirmed that most mast cells in nasal mucosae of 10 nasal allergic patients had c-kit receptor by immunohistochemistry using the mirror sectioning technique. We then investigated whether c-kit receptor+, tryptase-, IgE- cells existed in nasal mucosae of 15 nasal allergic patients and 15 nonallergic ones using sequential triple immunohistochemistry. We observed the area in which 1,000 to 1,100 tryptase-positive cells (mast cells) existed in both the subepithelial layer and the deep layer of each nasal lamina propria. The epithelial layer above this area was also examined. Some c-kit receptor+, tryptase- cells existed in the nasal mucosae of 11 patients with nasal allergy and of 5 patients with nonallergic rhinitis. From one to four of these cells in the nasal epithelium and subepithelial layer of the 4 allergic patients were IgE-negative. In contrast, no IgE-negative cells existed in the deep layer of allergic nasal mucosae or in any nonallergic nasal mucosae. Our results suggest that mast cell progenitors, hematopoietic progenitor cells or multipotential blood cells exist in the allergic nasal mucosa, and may contribute to the increase of mast cells in the epithelium and subepithelial layer of allergic nasal mucosa.

Proliferative activity of mast cells in allergic nasal mucosa.

The proliferative activity of mast cells in the nasal mucosae of allergic (n = 14) and non-allergic (n = 18) rhinopathic patients was studied by a sequential double immunohistochemistry using anti-proliferating cell nuclear antigen (PCNA) and anti-tryptase antibodies. Two hundred to 300 tryptase-positive cells (mast cells) were studied in each allergic nasal epithelium. In case of non-allergic nasal mucosa, only a few mast cells existed in the epithelial layer. The total number of mast cells which we could detect in all patients was 168 cells. One of these cells contained PCNA. Three hundred to 500 mast cells were studied in each subepithelial layer and deep layer of lamina propria of both diseases. PCNA-positive mast cells were observed in the nasal epithelia of 10 allergic patients. In the subepithelial layer, PCNA-positive mast cells were observed eight allergic patients and four non-allergic patients, respectively. In the deep lamina propria, PCNA-positive mast cells were observed in a few patients with both diseases. The percentage of PCNA-positive mast cells of all mast cells each area ranged from 0 to 1.7%. The incidence of PCNA-positive mast cells was statistically higher in the allergic epithelium and subepithelial layer than in the deep layer of lamina propria. Moreover, that of PCNA-positive mast cells in the subepithelial layer was higher in allergic than in non-allergic nasal mucosa. Our results suggest that mast cell proliferation may contribute to the number of mast cells in the nasal epithelium and subepithelial layer of allergic patients.