Pulmonary epithelioid haemangioendothelioma (PEH) is a rare pulmonary neoplasm. A patient with PEH with lymph node and pleural metastases that were discovered incidentally is described. An abnormal left upper lobe shadow was noticed on CXR in a 70-year-old woman during an assessment for the sudden onset of nausea and vomiting. Transbronchial lung biopsy did not provide a diagnosis. Lobectomy and lymph node resection were performed. The histological diagnosis of PEH was confirmed immunohistochemically by positive reactions to factor VIII-related antigen and CD34. Data on 93 patients with PEH including the present case report were analysed by Cox regression analysis using forward stepwise method to identify the risk factors, and the independent predictors of survival in patients with PEH. It revealed that male, symptomatic patients, presence of cough, haemoptysis, chest pain, multiple unilateral nodules, pleural effusion, metastases to more than one site and lymph node metastases were all significant risk factors for PEH (P<0.05). Symptomatic patients and presence of pleural effusion were the independent predictors of survival in patients with PEH.

Background Spasticity is a common complication of many neurological diseases and despite contributing much disability; the available therapeutic options are limited. Peripheral magnetic stimulation is one promising option. In this study, we investigated whether peripheral intermittent theta burst stimulation (piTBS) will reduce spasticity when applied directly on spastic muscles. Methods In this sham-controlled study, eight successive sessions of piTBS were applied directly to spastic muscles with supra threshold intensity. Assessment was done by modified Ashworth scale (mAS) and estimated Botulinum toxin dose (eBTD) at baseline and after the 8th session in both active and sham groups. Results A total of 120 spastic muscles of 36 patients were included in the analysis. Significant reduction of mAS and eBTD was found in the active compared to sham group (p < 0.001). The difference in mAS was also significant when tested in upper limb and lower limb subgroups. The degree of reduction in mAS was positively correlated with the baseline scores in the active group. Conclusion piTBS could be a promising method to reduce spasticity and eBTD. It consumes less time than standard high frequency protocols without compromising treatment efficacy. Trial registration: Clinical trial registry number: PACTR202009622405087. Retrospectively Registered 14th September, 2020.

Objective: The aim of the study was to examine the prophylactic role of repetitive transcranial magnetic stimulation (rTMS) on the frequency, and severity of migraine attacks in episodic migraineurs who failed medical treatment. Methods: A randomized double-blinded placebo-controlled study was designed to assess the effect of 5 Hz rTMS applied over the left dorsolateral prefrontal cortex (LDLPFC ) in 33 migraineurs. Patients were followed up for 1 month before receiving rTMS, and for another month after the sessions by a headache diary. The primary outcome measure was the achievement of 50% reduction in the number of migraine attacks. Secondary outcome measures included migraine days, assessment of migraine attack severity, disability by HIT-6, and side-effects to the procedure.Results: The study revealed that 69.2% of the active treatment group achieved 50% or more reduction in the number of migraine attacks versus 25% of cases in the control group (p = 0.02). The absolute number of migraine attacks was reduced by 3.1 vs 1.5 in the active and control group, respectively. The number of cases with severe HIT-6 scores was reduced by 46.2% in active treatment group versus a 7.1% reduction in the control group (p = 0.02). Conclusion: High-frequency rTMS applied to LDLPFC can reduce the number of migraine attacks by 50% or more in almost 70% of a sample of episodic migraineurs with a concomitant decrease in functional disability.

Although the histogenesis of sclerosing hemangioma (SH) of the lung is now thought to be respiratory epithelial in origin, the genetic abnormalities that mediate its development are not known. Because pathophysiology of several syndromes associated with benign tumors may converge on the tuberous sclerosis complex (TSC), serine/threonine kinase 11 (STK11), and mammalian target of rapamycin (mTOR) pathways, the purpose of the present paper was to investigate their roles in the development of SH. Semiquantitative immunohistochemical analysis was done to assess the expression of phospho-mTOR, phospho-S6 ribosomal protein, phosphatase and tensin homolog deleted on chromosome 10 (PTEN), phospho-Akt, STK11, tuberin, hamartin, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor-1alpha (HIF-1alpha) in 19 cases of typical SH. To determine whether genetic alteration of STK11 is involved in the development of SH, all encoding exons of STK11 were analyzed by polymerase chain reaction (PCR) amplification and direct sequencing of genomic DNA of six specimens. The six specimens were also investigated for whether promoter hypermethylation exists as an alternative inactivating mechanism for STK11. All specimens showed moderate to marked reaction to phospho-S6 ribosomal protein and PTEN; 16 specimens (84%) showed slight to moderate reaction to phospho-mTOR, negative reaction to STK11, and slight to moderate reaction to hamartin; 11 (58%) showed slight to moderate reaction to phospho-Akt; 18 (95%) showed slight to moderate reaction to tuberin and positive reaction for HIF-1alpha; and 17 (90%) showed moderate reaction to VEGF. No somatic mutation of STK11 was found and the six specimens were unmethylated in the promoter region. These data imply that aberrant mTOR signaling may play a role in the development of SH, and its vascular nature may be due partially to high levels of VEGF caused by dysregulation of mTOR signaling.

During a recent investigation of LKB1 gene abnormality in lung lesions, strong expression of LKB1 protein in normal neuroendocrine (NE) cells of the bronchial epithelium was found. Because LKB1 functions as a tumor suppressor gene, the question of whether alteration of LKB1 expression is related to the development of pulmonary NE tumors of various grades was investigated. LKB1 immunohistochemistry was examined in a total of 68 primary pulmonary NE tumors consisting of 30 specimens of small cell lung carcinoma (SCLC), 23 large cell neuroendocrine carcinomas (LCNEC), two atypical carcinoids, and 13 typical carcinoids. Loss or low expression (<20% immunoreactive cells) of LKB1 protein expression was more frequently observed in high-grade NE tumors (SCLC and LCNEC; 45/53, 84.9%) than in typical and atypical carcinoids (3/15; 20%). The difference in LKB1 immunoreactivity between the high-grade NE tumors and the carcinoid group was statistically significant (P < 0.0001). In conclusion, marked reduction of LKB1 expression in high-grade NE tumors of the lung suggests a possible role of LKB1 inactivation in its tumorigenesis. Although a few previous studies indicated rare genetic alterations of LKB1 in SCLC, further studies including analysis of other NE tumors and focusing on epigenetic abnormalities of LKB1 gene are warranted.