Selective posterior decompression of the cervical spine

Posterior decompression of the cervical spine is an accepted treatment for patients with cervical canal disease, but some patients experience postoperative axial pain and C5 or C6 palsy that affect their quality of life. Here we describe selective posterior decompression using a spinous process-splitting approach to prevent these complications performed in 17 patients with myelopathy treated at median 2.4 levels by selective posterior decompression via the transspinous approach. Clinical symptoms, axial pain, and C5 or C6 palsy were compared before and after treatment. The range of motion of the cervical spine and shift of the cervical cord were studied at the C5 level. All patients experienced symptom improvement and none suffered deterioration or required reoperation. The Japanese Orthopaedic Association score improved from 10.9 to 14.4 points and none of the patients reported C5 or C6 palsy or axial pain at the last follow-up visit. There was no statistically significant change in pre- and postoperative cervical alignment and range of motion. The posterior shift of the spinal cord at the C5 level was 1.7 mm. None of our 17 patients experienced significant postoperative axial pain after selective posterior decompression via the transspinous approach. Minimal spinal cord shift at the C5 level may have contributed to the reduced incidence of postoperative C5 or C6 palsy in our series. Selective posterior decompression is less invasive and effective in some patients with cervical canal disease.     

Lumbar canal stenosis with overactive bladder presenting urinary incontinence developed by walking: a case report

A 74-year-old male complained of lower back pain, paresthesia of the bilateral feet and urinary incontinence. Urinary incontinence manifested at rest and worsened with walking. He had a history of surgery for prostatic cancer. Lumbar magnetic resonance imaging (MRI) demonstrated lumbar canal stenosis at the L4/5 level. The investigations including a cystometrogram manifested an overactive bladder caused by lumbar canal stenosis. His clinical symptoms were unresponsive to conservative treatment and posterior decompression at the L4/5 level was performed surgically to treat lumbar canal stenosis. Postoperatively, his symptoms were relieved. Overactive bladder presenting urinary incontinence that deteriorates with walking due to lumbar canal stenosis is suspected of being caused by circulatory disturbance of the cauda equine or conus medullaris. Emergency treatment including surgery is required for urinary retention in patients with lumbar canal stenosis; however, some degree of urinary disturbance may persist even after prompt and adequate surgery. Overactive bladder such as the present case should be considered as a possible symptom of lumbar canal stenosis, and surgical treatment for lumbar canal stenosis may be considered in the 'overactive bladder' stage before urinary retention begins, if the patient does not respond to conservative treatment.     

Investigation of pharmacokinetics of crushed imidafenacin 0.1-mg tablet after single oral administration in healthy men

The crushing of tablets and opening of capsules should not be performed without proper care, as these actions may adversely affect the pharmaceutical release mechanisms. However, various clinical circumstances occasionally necessitate these actions. The long-term stability of the commercial formulation of imidafenacin was confirmed after crushing of tablets. For the safe administration of crushed imidafenacin tablets, we examined the pharmacokinetics of crushed imidafenacin 0. 1-mg tablet after single oral administration in healthy men. Plasma concentrations were measured in 6 male volunteers (age, 33.3 ± 10.6 years) orally administered crushed imidafenacin under fasting conditions. Imidafenacin was rapidly absorbed and plasma concentrations peaked (Cmax) at 414 ± 108 pg/ml after 1.5 h (Tmax ; median), after which the drug was rapidly eliminated with a half-life (t1/2) of 2.8 ± 0. 3 h. Area under the plasma concentration-time curve (AUC0-10) was 1,680 ± 334 pg?h/ml. There were no significant differences in Cmax, Tmax and t1/2 between the crushed and tablet medications. Thus, crushing has almost no influence on the pharmacokinetics of imidafenacin. Consequently, this study was made available as information for patients requiring crushed anticholinergic agents.     

Natural history of scoliosis in children with syringomyelia

We performed a retrospective review of 27 scoliotic patients with syringomyelia using MRI. Their mean age at the first MRI examination was 10.9 years, and at the final review 15.8 years. The mean ratio of the diameter of the syrinx to the cord on the midsagittal MRI (S/C ratio) decreased from 0.49 to 0.24; 14 patients showed a decrease of 50% or more (reduction group). In this reduction group, the cerebellar tonsillar herniation decreased from a mean of 11.3 mm to 6.0 mm, and some improvement in dissociated sensory disturbance was seen in nine of 13 patients. The scoliosis improved by 5 degrees or more in six patients in the reduction group. Our results indicate that spontaneous shrinkage of syringomyelia in children is not unusual and is associated with improvement in the tonsillar herniation, the scoliosis and the neurological deficit.     

Intracranial chondroma arising from the skull base: two case reports featuring the image findings for differential diagnosis

We reported two cases of intracranial skull base chondroma and discussed the differential diagnosis and the treatment strategies. The first case was a 39-year-old male who presented with left exophtalmos, visual loss and oculomotor disturbance. MRI showed a huge tumor occupying the bilateral cavernous sinus. Partial removal of the tumor was performed through the left orbitozygomatic subtemporal approach. The second case was a 54-year-old male who presented with left hemiparesis. MRI showed a brain stem infarction with a huge tumor located at the right middle fossa. Partial removal was performed through the right orbitozygomatic subtemporal approach. In these two cases, the histopathological diagnosis of the tumors was benign chondroma and the size of residual tumors have not changed for one year without any additional therapy. Although preoperative definite diagnosis for skull base chondromas is difficult, strategies for diagnosis and treatment without any complication are essential. In our cases, chondromas showed low uptake in PET images, which might be useful for differentiation between chondromas and chordomas. The current popular surgical approach for parasellar tumors is transcranial such as the orbitozygomatic subtemporal approach. In surgical removal of skull base chondromas, it is advisable to try to confirm the diagnosis preoperatively with characteristic image findings and to consider the best approach in each case to decompress the involved nerves without any complications.     

Acute lymphocytic leukemia recurring in the spinal epidural space

A 27-year-old man presented with a very rare spinal epidural mass associated with recurrence of acute lymphocytic leukemia (ALL) manifesting as acute progressive neurological deficits. The patient presented with shoulder pain and ambulatory difficulties 3 years after remission of ALL treated by bone marrow transplantation. Magnetic resonance imaging revealed an epidural mass extending from C-7 to T-3, which compressed the cord and extended to the intervertebral foramen along the roots. After decompression surgery, the symptoms dramatically improved. Histological examination showed clusters of immature lymphocytes consistent with recurrence of leukemia, so chemotherapy and radiation therapy were carried out. At 1 year after the operation, no local mass expansion or systemic progression of leukemia had occurred. Leukemic mass must be considered in the differential diagnosis of spinal epidural mass, even in patients with ALL.     

Hepatectomy-Related Hypophosphatemia: A Novel Phosphaturic Factor in the Liver-Kidney Axis

Marked hypophosphatemia is common after major hepatic resection, but the pathophysiologic mechanism remains unknown. We used a partial hepatectomy (PH) rat model to investigate the molecular basis of hypophosphatemia. PH rats exhibited hypophosphatemia and hyperphosphaturia. In renal and intestinal brush-border membrane vesicles isolated from PH rats, Na⁺-dependent phosphate (Pi) uptake decreased by 50%–60%. PH rats also exhibited significantly decreased levels of renal and intestinal Na⁺-dependent Pi transporter proteins (NaPi-IIa [NaPi-4], NaPi-IIb, and NaPi-IIc). Parathyroid hormone was elevated at 6 hours after PH. Hyperphosphaturia persisted, however, even after thyroparathyroidectomy in PH rats. Moreover, DNA microarray data revealed elevated levels of nicotinamide phosphoribosyltransferase (Nampt) mRNA in the kidney after PH, and Nampt protein levels and total NAD concentration increased significantly in the proximal tubules. PH rats also exhibited markedly increased levels of the Nampt substrate, urinary nicotinamide (NAM), and NAM catabolites. In vitro analyses using opossum kidney cells revealed that NAM alone did not affect endogenous NaPi-4 levels. However, in cells overexpressing Nampt, the addition of NAM led to a marked decrease in cell surface expression of NaPi-4 that was blocked by treatment with FK866, a specific Nampt inhibitor. Furthermore, FK866-treated mice showed elevated renal Pi reabsorption and hypophosphaturia. These findings indicate that hepatectomy-induced hypophosphatemia is due to abnormal NAM metabolism, including Nampt activation in renal proximal tubular cells.Inorganic phosphate (Pi) absorption in the renal proximal tubules and small intestine is important for Pi homeostasis.¹ The Na⁺-dependent Pi (Na/Pi) transport system includes type IIa and type IIc Na/Pi transporters, which are localized in the apical membrane of the proximal tubular cells, and type IIb Na/Pi transporters, which are localized in the apical membrane of the intestinal epithelial cells.^1,2 Pi (re)absorption is regulated by the dietary Pi content, parathyroid hormone (PTH), and the active metabolite of vitamin D, 1α, 25-dihydroxyvitamin D3 [1,25(OH)₂D₃].³ Other phosphaturic hormones, termed phosphatonins, also control renal Pi handling.⁴ The discovery that fibroblast growth factor (FGF) 23, the first identified phosphatonin,⁵ originated from osteocytes established the concept of the bone-kidney axis.^6,7The incidence of liver transplantation has steadily increased and the incidence of partial hepatectomy (PH) has also consequently increased.⁸ Hypophosphatemia frequently occurs after liver resection.^9–11 Acute hypophosphatemia causes septicemia and is associated with a poor prognosis.^11,12 Acute hypophosphatemia is of considerable clinical relevance because many hepatectomized patients develop marked hypophosphatemia and, thus, large doses of Pi replacement are required to maintain metabolic homeostasis.¹³ Urinary Pi excretion is markedly increased in many patients. After hepatectomy, hypophosphatemia is associated with hyperphosphaturia.¹³For many years, the increased metabolic demand of the regenerating liver was considered the underlying pathologic mechanism of hypophosphatemia. The magnitude of Pi uptake by the recovering liver, however, cannot explain the severity of the resulting hypophosphatemia.¹¹ Hepatectomy-induced hypophosphatemia is associated with an increased renal fractional excretion index for Pi unrelated to intact FGF23, FGF7, or secreted frizzled-related protein 4 as a phosphaturic factor,¹⁴ indicating that other factors have a role in the pathogenesis of hypophosphatemia.Nicotinamide (NAM) inhibits intestinal and renal Na/Pi transport activity in normal rats.^15–17 Administration of NAM to rats produces a specific dose-dependent inhibition of Na/Pi transport across the renal brush-border membrane (BBM) and an increase in urinary Pi excretion.^16,17 NAM suppresses hyperphosphatemia in hemodialysis patients.¹⁸ Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the first rate-limiting step in converting NAM to NAD,^19,20 which is essential for cellular metabolism, energy production, and DNA repair.^20–22 Nampt exists in two known forms: intracellular Nampt (iNampt) and secreted extracellular Nampt (eNampt).²³ eNampt also generates an intermediate product, nicotinamide mononucleotide (NMN).²³Our findings indicate that the acceleration of NAM metabolism through Nampt function in the kidney is involved in the hepatectomy-induced hypophosphatemia in rodent models. This study also suggests that NAM metabolism through the liver-kidney axis is important in Pi homeostasis.     

Outcome of sentinel lymph node biopsy in breast cancer using dye alone: a single center review with a median follow-up of 5 years

Purpose

Various techniques are used for sentinel lymph node biopsy (SLNB) in breast cancer. While subareolar injection with dye alone is a relatively easy method, few studies have reported the outcome with a follow-up period. This study presents our results of SLNB using dye alone.

Methods

Between November 2002 and December 2010, 701 patients with breast cancer underwent SLNB using subareolar injection of indocyanine green or indigo carmine. Sentinel lymph node (SLN)-negative patients were followed without axillary lymph node dissection (ALND).

Results

SLNs were detected in 654 of 701 patients (93.3 %), and the rate increased to 98.1 % over the course of the study. The mean number of SLNs removed was 1.5. There was no significant difference in the detection rate between two dyes. No adverse events resulted from the injection of dyes. Of the 654 patients, 136 (20.8 %) had SLN metastasis. Five hundred patients were followed without ALND. Thirty-six patients experienced disease relapse during a median follow-up of 60 months. Thirteen patients (2.6 %) had regional lymph node relapse, and eight of them could undergo salvage lymph node dissection. The 5-year disease-free and overall survival rates were 92.4 and 96.1 %, respectively.

Conclusion

SLNB using subareolar injection with dye alone was safe and feasible even after a long follow-up.     

Pheochromocytoma as the first manifestation of MEN2A with RET mutation S891A: report of a case

We report a rare case with pheochromocytoma as the first manifestation of multiple endocrine neoplasia type 2A with RET mutation S891A. Bilateral pheochromocytomas were identified in a 54-year-old woman. Screening for RET revealed a rare S891A mutation located in the intracellular tyrosine kinase domain. This mutation was previously recognized as one of the mutations only in cases manifesting solely medullary thyroid carcinomas (MTCs). Since calcitonin stimulation test indicated positive result, total thyroidectomy was performed 1 year after the bilateral adrenalectomy, and C-cell hyperplasia was diagnosed by histopathological examination. Our report suggests that cases with S891A mutation, akin to those with other RET mutations, require screening for pheochromocytoma. In addition, it is indicated that calcitonin stimulation test should be performed even in the unaffected elder cases with S891A mutation although the mutation is classified as lowest risk group on MTC in guidelines.