Background: Lateral elbow tendinopathy (LET) has an array of modalities described for its management. The present study analyzed two modalities used for managing the condition. Methods: The present study included 64 non-athletes with LET who failed conservative treatment that included avoiding strenuous activities, ice-fomentation, non-steroidal anti-inflammatory drugs, bracing, and physiotherapy for 6 months. A random allocation of the participants was done, with one group injected with platelet-rich plasma (PRP) and the other group with corticosteroids.The procedure was performed by the same blinded orthopedic surgeon after localizing the pathology using ultrasound. Visual analog scale (VAS) scores, disabilities of the arm, shoulder and hand (DASH) scores, Patient-Rated Tennis Elbow Evaluation (PRTEE) scores, and handgrip strengths were recorded by blinded observers other than the surgeon administering the injection. Results: The average age of the patients was 40 years. The mean VAS score at the latest follow-up of 2 years in the PRP group was 1.25 and it was significantly better than the score of 3.68 in the steroid group (p < 0.001). The mean DASH score at the latest follow-up of 2 years in the PRP group was 4.00 and it was significantly better than the score of 7.43 in the steroid group (p < 0.001).The mean PRTEE score at the latest follow-up of 2 years in the PRP group was 3.96 and it was significantly better than the score of 7.53 in the steroid group (p < 0.001). The scores were better in the steroid group at a short-term follow-up of 3 months (p < 0.05), while they were better in the PRP group at a long-term follow-up of 2 years (p < 0.05). Hand-grip strength was comparable in the PRP group (84.43 kg force) and steroid group (76.71 kg force) at the end of the 2-year follow-up with no statistically significant difference (p = 0.149). Conclusions Corticosteroid injections alleviated symptoms of LET over short-term follow-up providing quicker symptomatic relief; however, the effect faded off over the long term. PRP injections provided a more gradual but sustained improvement over the longterm follow-up, indicating the biological healing potential of PRP.

Objective: Recessive variants in the PINK1 gene are known causes of early-onset Parkinson’s disease (EOPD). To describe the clinical features and genetic profiles of patients with PINK1-related Parkinson’s disease (PARK-PINK1) mutations. Methods: We conducted a retrospective chart review of the demographic, clinical and genetic details of patients from our database carrying biallelic PINK1 variants. Results: A total of 7 patients whose median age at onset was 33 years (range: 20–49) were recruited. All had asymmetrical onset, tremors were present in 4 patients, abnormal posturing was present in 2 patients, and slowness was present in 1 patient. The parkinsonism phenotype was noted in 6 patients (with dystonia in four) and isolated dystonia in one. Among the 6 patients with parkinsonism, five had rest tremors, all had good levodopa responses, and four had motor fluctuations with choreiform dyskinesia. Exome sequencing revealed biallelic pathogenic/likely pathogenic variants, five of which were novel. Conclusion PARK-PINK1 presents as an EOPD with tremor-predominant phenotype, good levodopa-responsiveness, early motor fluctuation and dyskinesia. We describe five novel variants in PINK1 gene.

Objective: Recessive variants in the PINK1 gene are known causes of early-onset Parkinson’s disease (EOPD). To describe the clinical features and genetic profiles of patients with PINK1-related Parkinson’s disease (PARK-PINK1) mutations. Methods: We conducted a retrospective chart review of the demographic, clinical and genetic details of patients from our database carrying biallelic PINK1 variants. Results: A total of 7 patients whose median age at onset was 33 years (range: 20–49) were recruited. All had asymmetrical onset, tremors were present in 4 patients, abnormal posturing was present in 2 patients, and slowness was present in 1 patient. The parkinsonism phenotype was noted in 6 patients (with dystonia in four) and isolated dystonia in one. Among the 6 patients with parkinsonism, five had rest tremors, all had good levodopa responses, and four had motor fluctuations with choreiform dyskinesia. Exome sequencing revealed biallelic pathogenic/likely pathogenic variants, five of which were novel. Conclusion PARK-PINK1 presents as an EOPD with tremor-predominant phenotype, good levodopa-responsiveness, early motor fluctuation and dyskinesia. We describe five novel variants in PINK1 gene.

Objective: Recessive variants in the PINK1 gene are known causes of early-onset Parkinson’s disease (EOPD). To describe the clinical features and genetic profiles of patients with PINK1-related Parkinson’s disease (PARK-PINK1) mutations. Methods: We conducted a retrospective chart review of the demographic, clinical and genetic details of patients from our database carrying biallelic PINK1 variants. Results: A total of 7 patients whose median age at onset was 33 years (range: 20–49) were recruited. All had asymmetrical onset, tremors were present in 4 patients, abnormal posturing was present in 2 patients, and slowness was present in 1 patient. The parkinsonism phenotype was noted in 6 patients (with dystonia in four) and isolated dystonia in one. Among the 6 patients with parkinsonism, five had rest tremors, all had good levodopa responses, and four had motor fluctuations with choreiform dyskinesia. Exome sequencing revealed biallelic pathogenic/likely pathogenic variants, five of which were novel. Conclusion PARK-PINK1 presents as an EOPD with tremor-predominant phenotype, good levodopa-responsiveness, early motor fluctuation and dyskinesia. We describe five novel variants in PINK1 gene.

Objective: Recessive variants in the PINK1 gene are known causes of early-onset Parkinson’s disease (EOPD). To describe the clinical features and genetic profiles of patients with PINK1-related Parkinson’s disease (PARK-PINK1) mutations. Methods: We conducted a retrospective chart review of the demographic, clinical and genetic details of patients from our database carrying biallelic PINK1 variants. Results: A total of 7 patients whose median age at onset was 33 years (range: 20–49) were recruited. All had asymmetrical onset, tremors were present in 4 patients, abnormal posturing was present in 2 patients, and slowness was present in 1 patient. The parkinsonism phenotype was noted in 6 patients (with dystonia in four) and isolated dystonia in one. Among the 6 patients with parkinsonism, five had rest tremors, all had good levodopa responses, and four had motor fluctuations with choreiform dyskinesia. Exome sequencing revealed biallelic pathogenic/likely pathogenic variants, five of which were novel. Conclusion PARK-PINK1 presents as an EOPD with tremor-predominant phenotype, good levodopa-responsiveness, early motor fluctuation and dyskinesia. We describe five novel variants in PINK1 gene.