Treatment of vasospasm by balloon angioplasty: experimental studies and clinical experiences

Abstract

The vasodilation mode and degree of the invasion caused by balloon angioplasty were experimentally examined. Assessment by light microscopy and scanning electron microscopy demonstrated that the invasion to the implanted arterial wall, taken from a patient who died from vasospasm, was minimized by the use of the balloon under the condition at 1 atm, 10 times for 10 seconds. Furthermore, we applied angioplasty to eight patients who developed severe vasospasm after subarachnoid haemorrhage, and five showed improvement in neuro-physiological (transcranial Doppler sonography), neuroradiological, and clinical examinations. In addition, blood vessels obtained from one patient who died 10 days after angioplasty, demonstrated similar findings to those of the experimental studies. It can be said that angioplasty will be one of the effective therapeutic methods to manage vasospasm when it is applied under the conditions mentioned above.     

Jaw Opening and Swallow Triggering Method for Bilateral-Brain-Damaged Patients: K-Point Stimulation

The aim of this study was to confirm the response in patients stimulated at the trigger point (K-point). Since we have already clinically encountered patients with hyperactive bite reflexes who were able to open their mouth and swallow after stimulation of the trigger point, we investigated this response in other brain-damaged patients. The trigger point lies on the mucosa lateral to the palatoglossal arch and medial to the pterygomandibular fold at the height of the postretromolar pad. A total of 57 brain-damaged patients, including patients with pseudobulbar palsy due to bilateral upper motor neuron disease and bulbar palsy due to medulla oblongate. Other supratentorial brain-damaged patients and 20 non-brain-damaged subjects were also examined. The subjects were gently stimulated at the trigger point by a finger or a tongue depressor. We found that the pseudobulbar palsy patients with a hyperactive bite reflex responded by mouth opening and swallowing after a jaw movement similar to mastication elicited by the stimulation. The other pseudobulbar palsy patients, who did not have hyperactive bite reflexes and could open their mouth spontaneously, responded by swallowing with jaw movements similar to mastication after the stimulation. The bulbar palsy patients and the supratentorial brain-damaged patients showed no response to the stimulation. The non-brain-damaged subjects also did not respond, but all of the subjects reported a strange sensation after the stimulation. We concluded that stimulating the trigger point was useful for opening the mouth and facilitating swallowing in pseudobulbar palsy patients and that this technique may be of help in these patients in terms of oral health care and feeding.     

Highly sensitive and quantitative evaluation of the EGFR T790M mutation by nanofluidic digital PCR

The mutation of T790M in EGFR is a major mechanism of resistance to treatment with EGFR-TKIs. Only qualitative detection (presence or absence) of T790M has been described to date, however. Digital PCR (dPCR) analysis has recently been applied to the quantitative detection of target molecules in cancer with high sensitivity. In the present study, 25 tumor samples (13 obtained before and 12 after EGFR-TKI treatment) from 18 NSCLC patients with activating EGFR mutations were evaluated for T790M with dPCR. The ratio of the number of T790M alleles to that of activating mutation alleles (T/A) was determined. dPCR detected T790M in all 25 samples. Although T790M was present in all pre-TKI samples from 13 patients, 10 of these patients had a low T/A ratio and manifested substantial tumor shrinkage during treatment with EGFR-TKIs. In six of seven patients for whom both pre- and post-TKI samples were available, the T/A ratio increased markedly during EGFR-TKI treatment. Highly sensitive dPCR thus detected T790M in all NSCLC patients harboring activating EGFR mutations whether or not they had received EGFR-TKI treatment. Not only highly sensitive but also quantitative detection of T790M is important for evaluation of the contribution of T790M to EGFR-TKI resistance.     

Thoracoscopic hepatectomy for malignant liver tumor

Background

Anatomical position of the liver poses a difficulty in approaching the lesions using a laparoscopic approach.

Methods

The patient was a 79-year-old man with a surgical history of laparoscopic sigmoidectomy for colon cancer and posterior segmentectomy of the liver for metastatic liver tumor. On admission, he presented with another liver tumor (diameter, 1.5 cm) in the dome of segment VIII. Because of the high possibility of severe adhesion around the liver and difficulty of approaching the lesion from the abdomen, we selected the transthoracic approach rather than the abdominal approach; the patient consented to this procedure. The patient was placed in the left-lateral position under general anesthesia with single-lung ventilation. We placed three trocars into the right thoracic space. The intrathoracic space was observed using a flexible-tip rigid scope (Olympus, Tokyo, Japan). The tumor was detected by inserting a flexible laparoscopic ultrasound probe (Hitachi Aloka, Ltd., Tokyo, Japan) through the diaphragm; the diaphragm was dissected immediately above the tumor using a harmonic scalpel (Ethicon Endo-Surgery, Inc., Cornelia, GA). The liver surface was precoagulated using a low-voltage monopolar coagulator with a ball-shaped tip (Amco Inc., Tokyo, Japan) with the electrosurgical unit VIO300D (Erbe Elektromedizin, Tuebingen, Germany). The parenchyma was first sealed using BiClamp LAP forceps (Erbe Elektromedizin) and divided using the harmonic scalpel. The specimen was extracted using a retrieval bag. After complete hemostasis was achieved, the diaphragm was closed by continuous suturing.

Results

The operation lasted for 310 min and estimated blood loss was 10 mL. The patient was discharged on postoperative day 4.

Conclusions

Although the duration of TH was long because of the narrow thoracic cavity space, TH was performed without any problems. As a rule, we should select TH for lesions located in the dorsal segment VII/VIII, with severe adhesion around the liver.     

18F-FDG uptake on PET in primary mediastinal non-thymic neoplasm: a clinicopathological study

Background

The usefulness of 2-[¹⁸F]-fluoro-2-deoxy-d-glucose (¹⁸F-FDG) positron emission tomography (PET) has been investigated in thymic epithelial tumors. However, little is known about PET imaging of ¹⁸F-FDG in primary non-thymic mediastinal neoplasms. The aim of this study is to explore the clinicopathological significance of ¹⁸F-FDG PET in primary mediastinal (non-thymic) neoplasms.

Methods

Twenty-one patients with mediastinal neoplasms who underwent ¹⁸F-FDG PET before treatment were included in this study. Tumor sections were stained by immunohistochemistry for glucose transporter 1 (Glut1); glucose transporter 3 (Glut3); hypoxia-inducible factor-1 alpha (HIF-1α); hexokinase I; vascular endothelial growth factor (VEGF); microvessels (CD34); epidermal growth factor receptor (EGFR); Akt/mTOR signaling pathway (p-Akt and p-mTOR); cell cycle control (p53).

Results

Seventeen of 21 patients were imaged on PET system using ¹⁸F-FDG, but 4 patients with a histology of cyst showed nothing abnormal in PET scans. The histology of the resected tumors was as follows: 6 schwannoma, 3 teratoma, 4 cyst, 3 sarcoma, 1 undifferentiated carcinoma, 1 seminoma, 1 mediastinal goiter, 1 ganglioneuroma, and 1 Hodgkin lymphoma. ¹⁸F-FDG uptake was significantly correlated with Glut1, HIF-1α, EGFR, p-Akt and p-S6K. These biomarkers were highly expressed in schwannoma, teratoma and high grade malignancies, whereas all patients with cyst and ganglioneuroma had no positive expression of these biomarkers. High uptake of ¹⁸F-FDG was significant associated with Glut1, VEGF, EGFR, p-Akt, p-S6K and tumor maximal size.

Conclusion

The amount of ¹⁸F-FDG uptake in primary mediastinal non-thymic neoplasms is determined by the presence of glucose metabolism (Glut1), hypoxia (HIF-1α) and upstream components of HIF-1α (EGFR, p-Akt and p-S6K).