Metastasis over implantable venous access ports.

BACKGROUND: The totally implantable venous access port (TIVAP) is an important device for patients receiving chemotherapy. We have reported, to our knowledge, the first case of a metastatic tumor over a TIVAP implanted via the Seldinger technique with a subclavian vein puncture. METHODS: Our patient, a 48-year-old man with hard palate cancer, had metastasis over the TIVAP. CT studies showed that the tumor had spread along the catheter from the neck to the chest wall. RESULTS: The cause of death was multiple lung metastases and intractable tumor bleeding over the TIVAP. CONCLUSIONS: We present a novel case of metastasis over the TIVAP implanted by use of the Seldinger technique. This technique is used for patients receiving prolonged cytotoxic therapy for malignancy. Although the Seldinger technique is quick and more effective, we prefer the cephalic vein cut-down technique when an aggressive, advanced cancer of head and neck is involved.

Assessment of gentamicin-induced vestibulotoxicity by click and galvanic vestibular-evoked myogenic potentials: a guinea pig investigation.

OBJECTIVE: The aim of this investigation carried out with guinea pigs was to study the possible effects of a gentamicin treatment on the saccular macula and on its afferent vestibular ganglion neurons. METHODS: The gentamicin-induced impairment was analyzed using vestibular-evoked myogenic potentials (VEMPs) elicited by both click and galvanic vestibular stimulations (GVS). Fifty microl of saline or gentamicin solution (40 mg/ml) was dropped over the round window membrane of the right (control) and left (lesion) cochleae, respectively. Four weeks after surgery, the VEMPs elicited with clicks and GVS were evaluated for each animal. Then, the animals were sacrificed in order to perform morphological and anti-Nav1.8 immunocytochemical analyses. RESULTS: Click- and GVS-VEMPs were obtained in all of the controls, whereas no potentials were obtained from gentamicin-treated animals. Lesions of sensory cells were observed in the saccular macula. In the injured vestibular ganglion, the percentage of voltage-gated sodium channel Nav1.8-like immunoreactive (Nav1.8-LI) neurons was significantly lower (38.9+/-0.7) than that (53.6+/-3.2) calculated in controls. CONCLUSIONS: Gentamicin-induced impairments of the saccular macula and afferents of guinea pigs can be evaluated by recording both click- and GVS-VEMPs. Both tests provide information on the sacculo-collic reflex pathway and could help a clinical diagnosis of gentamicin intoxication by conventional eardrops in the patient with a perforated eardrum.

Vestibular evoked myogenic potentials are heavily dependent on type I hair cell activity of the saccular macula in guinea pigs.

This study applied the vestibular evoked myogenic potential (VEMP) test to guinea pigs coupled with electronic microscopic examination to determine whether VEMPs are dependent on type I or II hair cell activity of the saccular macula. An amount of 0.05 ml of gentamicin (40 mg/ml) was injected directly overlaying, but not through, the round window membrane of the left ear in guinea pigs.One week after surgery, auditory brainstem response test revealed normal responses in 12 animals (80%), and elevated thresholds in 3 animals (20%). The VEMP test using click stimulation showed absent responses in all 15 animals (100%). Another 6 gentamicin-treated animals underwent the VEMP test using galvanic stimulation and all 6 also displayed absent responses. Ultrathin sections of the saccular macula in the gentamicin-treated ears displayed morphologic alterations in type I or II hair cells, including shrinkage and/or vacuolization in the cytoplasm, increased electron density of the cytoplasm and nuclear chromatin, and cellular lucency. However, extrusion degeneration was rare and only present in type II hair cells. Quantitative analysis demonstrated that the histological density of intact type I hair cells was 1.1 +/- 1.2/4000 microm(2) in the gentamicin-treated ears, showing significantly less than that in control ears (4.5 +/- 1.8/4000 microm(2)). However, no significant difference was observed in the densities of intact type II hair cells and supporting cells between treated and control ears. Furthermore, the calyx terminals surrounding the damaged type I hair cells were swollen and disrupted, while the button afferents contacting the damaged type II hair cells were not obviously deformed. Based on the above results, we therefore conclude that VEMPs are heavily dependent on type I hair cell activity of the saccular macula in guinea pigs.

Physiological and morphological assessment of the saccule in Guinea pigs after noise exposure.

OBJECTIVE: To investigate whether the saccule exhibits temporary or permanent functional loss resembling threshold shifts in auditory brainstem response (ABR) of guinea pigs following noise exposure. DESIGN: Randomly bred guinea pigs were divided into 3 groups: A (short-term noise exposure, 30 minutes, n = 15), B (long-term noise exposure, 40 hours, n = 9), and C (no noise exposure, n = 5). SETTING: University hospital. MAIN OUTCOME MEASURES: All animals underwent vestibular-evoked myogenic potential (VEMP) and ABR tests. Chronological changes of VEMP and ABR responses following noise exposure were analyzed and compared. After audiovestibular function testing, animals were killed for morphological study with light and electron microscopy. RESULTS: In group A, temporary VEMP loss and ABR threshold shifts recovered 2 and 4 days, respectively, after short-term noise exposure, with an interval of 2 days earlier in the recovery of VEMPs than that of ABR thresholds. In contrast, in group B, 78% and 83% of the ears exhibited permanent VEMP loss and ABR threshold shifts, respectively, 10 days following long-term noise exposure. In group C, all animals showed normal VEMPs and ABRs throughout the study period. Light and electron microscopic studies confirmed that loss of VEMPs correlated with saccular lesion. CONCLUSIONS: The saccule can exhibit temporary or permanent functional loss resembling hearing threshold shifts in guinea pigs following noise exposure. Recovery of VEMP precedes restoration of hearing threshold after damage from short-term noise exposure. Conversely, permanent VEMP loss after long-term noise exposure may reflect permanent hearing threshold shifts.

Correlating the cochleovestibular deficits with tumor size of acoustic neuroma.

CONCLUSION: The tumor size of acoustic neuroma correlates with cochleovestibular deficits. Those tumors with global frequency hearing loss, bilateral gaze nystagmus, or absent caloric and VEMP responses may indicate a tumor size >2.5 cm. OBJECTIVE: This study aimed to investigate the correlation between cochleovestibular deficits and the size of acoustic neuroma. PATIENTS AND METHODS: A total of 44 patients with acoustic neuroma were enrolled in this study. Pure tone audiometry, electronystagmography, caloric test, vestibular evoked myogenic potential (VEMP) test, and MRI were conducted. RESULTS: There is a trend of correlation between tumor size and audiographic configuration, with small-sized tumor in normal and rising types, medium-sized tumor in mid- and high-frequency hearing loss, and large-sized tumor in flat and deafness types. Five patients with bilateral gaze nystagmus had significantly larger tumor size than those without nystagmus. When 1 and 0 are used to represent abnormal and normal responses, respectively, the relationship between tumor size and vestibular function can be expressed as: tumor size (cm)=1.43 (caloric response)+1.35 (VEMP response), indicating that the estimated tumor size for those with abnormal caloric or VEMP responses increased by 1.43 or 1.35 cm, respectively.

Effect of intratympanic application of aminoglycosides on click-evoked myogenic potentials in Guinea pigs.

OBJECTIVES: Although numerous studies have identified damage to the cochlear and vestibular end organs as the primary site of aminoglycoside-induced ototoxicity, the effect on the saccule remains poorly understood, possibly due to lack of monitoring saccular function in experimental animals. Therefore, this study applied three kinds of aminoglycosides into the tympanic space of guinea pigs to examine their toxic impact on the saccule by way of click-evoked myogenic potential test coupled with morphologic assessment. DESIGN: Albino guinea pigs were treated with saline, gentamicin, tobramycin, or amikacin, with 10 animals assigned to each group. Each compound was injected directly overlying but not through the round window membrane on the left ear, with the right ear serving as a control. One week after injection, each animal underwent auditory brain stem response, caloric test, and click-evoked myogenic potential test. Animals were then killed for morphologic assessment through the use of light and electron microscopic examinations. RESULTS: The animals treated with saline, gentamicin, tobramycin, or amikacin exhibited abnormal auditory brain stem response in 0%, 30%, 100%, and 30% of cases; abnormal caloric responses were found in 0%, 100%, 40%, and 40% of cases; absent click-evoked myogenic potentials were found in 0%, 100%, 30%, and 40% of cases, respectively. Gentamicin and other groups differed significantly in abnormal rates of caloric responses and click-evoked myogenic potentials. Morphologic study of the gentamicin-treated animals confirmed that the absence of click-evoked myogenic potential originated from the lesion in the saccular macula. CONCLUSIONS: Gentamicin represents the dominant susceptibility of aminoglycoside-induced vestibulotoxicity for eliminating both semicircular canal and saccular functions. This study further confirms the findings of human studies in which the caloric and vestibular evoked myogenic potentials responses were monitored to assess the abolition of vestibular function in patients treated with intratympanic gentamicin injection.

Over-expression of c-kit in a primary leiomyosarcoma of the thyroid gland.

Primary leiomyosarcoma of the thyroid gland is rare. In this paper, we report a case of high-grade leiomyosarcoma of the thyroid gland in a 43-year-old man. Lung metastasis was also noted in this patient. Despite of aggressive surgical treatment, the patient died of uncontrolled local recurrent disease 6 months after the initial operation. Immunohistochemical studies showed the tumor cells were positive for c-kit proto-oncogene product. Imatinib mesylate was used as a post-operative adjuvant treatment but the response was poor. The role of tyrosine kinase inhibitors on the treatment of thyroid leiomyosarcomas is still unclear because this is the first report of c-kit over-expression in such tumors. Nevertheless, our results show that c-kit over-expression might not be an indicator of good response to imatinib mesylate treatment in thyroid leiomyosarcomas.

A time course analysis of the changes in neuropeptide Y immunoreactivity in the rat cuneate nucleus following median nerve transection.

Using median nerve injury and immunocytochemical methods, we examined the temporal changes in neuropeptide Y (NPY) expression in the cuneate nucleus (CN) in rats following median nerve transection. Under normal circumstances, neuropeptide Y-immunoreactive (NPY-IR) fibers was not detectable in the CN. A few NPY-IR fibers were observed in the ipsilateral CN 5 days after the median nerve transection, and peaked at 4 weeks. Thereafter, they were gradually returned to nearly control level after 16 weeks. Quantitative evaluation showed that the mean percentage of area occupied by NPY-IR fibers in entire and three subregions of the CN at 4 weeks were significantly higher than that at other post-operated time points, respectively. The present ultrastructural observations in the middle region of CN showed that the significantly increased NPY immunoreactivity was confined only in the myelinated axons and terminals but not detected in the dendrites, somata, and glial cells. The NPY-IR terminals made axodendritic synaptic contacts with unlabeled elements. The present results indicate that the time course of the increase of NPY immunoreactivity is similar to c-Fos expression as described in a previous study. It is speculated that the increased NPY in the CN after axotomy may affect the excitability of postsynaptic cuneate neurons, however, the functional interaction between NPY and c-Fos-IR neurons needs to be further studied.

Changes in c-Fos protein expression in the rat cuneate nucleus after electric stimulation of the transected median nerve.

In this study we investigate temporal changes in Fos expression in cuneate neurons after a high-threshold electrical stimulation of the transected median nerve in rats. Two hours after injury of the median nerve when given electrical stimulation, c-Fos-immunoreactive (c-Fos-IR) cells were barely detected in the ipsilateral cuneate nucleus (CN). A few c-Fos-IR cells, however, were observed in the ipsilateral CN at 5 days. A marked increase in c-Fos-IR cells was observed at 2, 3, and 4 weeks, but levels subsided thereafter. Labeled cells were totally diminished by 16 weeks. The statistical analysis showed that the mean density of c-Fos-IR cells throughout the CN at 4 weeks was significantly higher than at other post-surgical time points, except for 3 weeks. Furthermore, the mean density of c-Fos-IR cells in the middle region of the CN was markedly higher than in other areas of the nucleus. The mean density of c-Fos-IR cells in the middle region at 4 weeks (mean density = 35.9 +/- 3.0 cells/section) was considerably higher than at other time points. Combined retrograde Fluorogold (FG) labeling and c-Fos immunocytochemistry showed that throughout the CN about 60% (2270/3652) of the c-Fos-IR cells contained FG, confirming that they were cuneothalamic projection neurons (CTNs). Moreover, the percentage of double-labeled cells in the middle region at 2 weeks (78.9 +/- 0.6%) was significantly greater than at 3 (70.2 +/- 3.4%) and 4 weeks (66.0b +/- 1.4%) after injury. Although the mechanism leading to the vigorous c-Fos expression in the CTNs following the electrical stimulation of the transected median nerve remains unclear the hyperexcitable CTNs may transmit the neuropathic nociceptive sensation to the thalamus after the median nerve injury.