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Neuromuscul Disord 2019 Feb 25. Epub 2019 Feb 25.

Division of Neurochemistry, Institute of Experimental Epileptology and Cognition Research, University of Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany; Department of Epileptology, University of Bonn, Germany. Electronic address:

Chronic progressive external ophthalmoplegia (CPEO) is a frequent clinical manifestation of disorders caused by pathogenic mitochondrial DNA mutations. However, for diagnostic purposes skeletal muscle tissue is used, since extraocular muscle tissue is usually not available for work-up. In the present study we aimed to identify causative factors that are responsible for extraocular muscle to be primarily affected in CPEO. Read More

Case Rep Neurol Med 2019 6;2019:5918632. Epub 2019 Mar 6.

Department of Clinical and Experimental Medicine, Neurological Clinic, University of Pisa, Pisa, Italy.

The classic features of deoxyguanosine kinase () deficiency are infantile onset hepatic failure with nystagmus and hypotonia; mitochondrial DNA studies on affected tissue reveal mitochondrial DNA depletion. Later, it has been shown that the mutations in the same gene may present with adult-onset mitochondrial myopathy and mitochondrial DNA multiple deletions in skeletal muscle. Here we report the case of a 42-year-old Italian woman presenting with a chronic progressive external ophthalmoplegia and myopathy with mtDNA multiple deletions and the compound heterozygous c. Read More

BMJ Case Rep 2019 Mar 31;12(3). Epub 2019 Mar 31.

Neurology Department, Centro Hospitalar de Lisboa Ocidental EPE, Lisboa, Portugal.

Mutations in the nuclear POLG1 gene compromise the integrity of mitochondrial DNA and show great allelic and clinical heterogeneity. Among adult POLG1-associated mitochondrial disease, the main clinical feature is chronic progressive external ophthalmoplegia. Other related clinical manifestations are sensory or cerebellar ataxia, peripheral neuropathy, myopathy or extrapyramidal symptoms. Read More

J Neurol 2019 Apr 2;266(4):953-959. Epub 2019 Feb 2.

Neurological Clinic, University of Pisa, Pisa, Italy.

Muscle pain may be part of many neuromuscular disorders including myopathies, peripheral neuropathies and lower motor neuron diseases. Although it has been reported also in mitochondrial diseases (MD), no extensive studies in this group of diseases have been performed so far. We reviewed clinical data from 1398 patients affected with mitochondrial diseases listed in the database of the "Nation-wide Italian Collaborative Network of Mitochondrial Diseases", to assess muscle pain and its features. Read More

Neurology 2019 Jan;92(4):e394

From the Departments of Neurology (A.M.P., S.H.M., R.D.), Ophthalmology (M.D.A.), and Clinical Genomics (R.D.), Mayo Clinic, Scottsdale, AZ.

Nervenarzt 2019 Feb;90(2):121-130

Friedrich-Baur-Institut an der Neurologischen Klinik und Poliklinik, Klinikum der Universität München, Ziemssenstr. 1, 80336, München, Deutschland.

Mitochondrial diseases (MD) are caused by mutations in the mitochondrial DNA or nuclear DNA. The clinical manifestation is often most severe in tissues with high energy demands. The most common MDs are Leber's hereditary optic neuropathy (LHON), chronic progressive external ophthalmoplegia (CPEO) and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). Read More

Adv Exp Med Biol 2018;1085:161-162

Department of Ophthalmology, Columbia University, Edward S. Harkness Eye Institute, NewYork-Presbyterian Hospital, New York, NY, USA.

Mitochondrial diseases are multisystem disorders: anemia, myopathy, lactic acidosis, CNS abnormality, endocrine abnormalities, renal disease, sensorineural deafness, and retinal involvement. The clinical abnormalities are heterogeneous, and they usually begin in childhood. Premature death occurs because of cardiac conduction defects. Read More

Gene 2019 Mar 5;688:171-181. Epub 2018 Dec 5.

Department of Neurology and Paediatrics, Centro Médico Nacional Siglo XXI, IMSS, Mexico City, Mexico.

Mitochondria both produce the energy of the cell as ATP via respiration and regulate cellular metabolism. Accordingly, any deletion or mutation in the mitochondrial DNA (mtDNA) may result in a disease. One of these diseases is Kearns Sayre syndrome (KSS), described for the first time in 1958, where different large-scale deletions of different sizes and at different positions have been reported in the mitochondrial genome of patients with similar clinical symptoms. Read More

Yonsei Med J 2018 Dec;59(10):1190-1196

Department of Pediatrics, Gangnam Severance Hospital, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea.

Purpose: To evaluate the classification, diagnosis, and natural course of ophthalmoplegia associated with mitochondrial disease.

Materials And Methods: Among 372 patients with mitochondrial disease who visited our hospital between January 2006 and January 2016, 21 patients with ophthalmoplegia were retrospectively identified. Inclusion criteria included onset before 20 years of age, pigmentary retinopathy, and cardiac involvement. Read More

Can J Ophthalmol 2018 10 17;53(5):e203-e205. Epub 2018 Feb 17.

Northampton General Hospital NHS Trust, Northampton, United Kingdom.

Cardiol Young 2018 Dec 17;28(12):1487-1488. Epub 2018 Oct 17.

1Department of Cardiology,Children's Hospital of Pittsburgh of UPMC,Pittsburgh, PA,USA.

Cardiac conduction disease affects patients with Kearns-Sayre syndrome. We report a young asymptomatic patient with Kearns-Sayre syndrome with abnormal conduction on electrocardiogram and Holter monitor, although not advanced atrioventricular block. She underwent prophylactic pacemaker placement, and rapidly developed complete atrioventricular block, which resulted in 100% ventricular pacing. Read More

BMJ Case Rep 2018 Oct 2;2018. Epub 2018 Oct 2.

Department of Ophthalmology, Dr Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India.

Fortschr Neurol Psychiatr 2018 09 24;86(9):584-591. Epub 2018 Sep 24.

Ludwig-Maximilians-Universität München, Friedrich- Baur-Institut der Neurologischen Klinik.

Mitochondrial diseases (MD) represent a heterogenous group of disorders and syndromes caused either by mutations of the mitochondrial DNA (mtDNA) or the nuclear DNA (nDNA). They belong to the most frequent neurogenetic diseases. The spectrum of clinical manifestations is very broad ranging from mild subclinical presentations to rapidly progressive debilitating conditions with reduced life expectancy. Read More

Mitochondrion 2018 11 6;43:37-42. Epub 2018 Aug 6.

Department of Pediatrics and Pediatric Neurology, University Medical Center Göttingen, Georg-August-Universität Göttingen, Göttingen, Germany.

Kearns-Sayre syndrome (KSS) is a multisystemic disorder marked by aerobic cell metabolism dysfunction. Fibroblasts derived from KSS patient skin biopsy exhibit heterogeneous occurrence of mitochondrial genomes as those circular DNA molecules partially carry the common deletion. In our approach, we aim to evaluate the intercellular alterations in respect to mitochondrial DNA integrity by laser capture microdissection and multiplex quantitative real-time PCR in single cells. Read More

Top Magn Reson Imaging 2018 Aug;27(4):219-240

Department of Radiology, University of Pittsburgh School of Medicine, Director of Pediatric Neuroradiology, Children Hospital of Pittsburgh, Pittsburgh, PA.

Mitochondrial diseases are a complex and heterogeneous group of genetic disorders that occur as a result of either nuclear DNA or mitochondrial DNA pathogenic variants, leading to a decrease in oxidative phosphorylation and cellular energy (ATP) production. Increasing knowledge about molecular, biochemical, and genetic abnormalities related to mitochondrial dysfunction has expanded the neuroimaging phenotypes of mitochondrial disorders. As a consequence of this growing field, the imaging recognition patterns of mitochondrial cytopathies are continually evolving. Read More

Essays Biochem 2018 07 20;62(3):235-254. Epub 2018 Jul 20.

IRCCS Institute of Neurological Sciences of Bologna, Bellaria Hospital, Bologna, Italy.

The landmark year 1988 can be considered as the birthdate of mitochondrial medicine, when the first pathogenic mutations affecting mtDNA were associated with human diseases. Three decades later, the field still expands and we are not 'scraping the bottom of the barrel' yet. Despite the tremendous progress in terms of molecular characterization and genotype/phenotype correlations, for the vast majority of cases we still lack a deep understanding of the pathogenesis, good models to study, and effective therapeutic options. Read More

PLoS One 2018 18;13(6):e0199258. Epub 2018 Jun 18.

UMR 7156 Génétique Moléculaire, Génomique, Microbiologie (GMGM), Strasbourg University-CNRS, Strasbourg, France.

Mutations in mitochondrial DNA are an important source of severe and incurable human diseases. The vast majority of these mutations are heteroplasmic, meaning that mutant and wild-type genomes are present simultaneously in the same cell. Only a very high proportion of mutant mitochondrial DNA (heteroplasmy level) leads to pathological consequences. Read More

Mol Psychiatry 2018 Oct 11;23(10):2039-2049. Epub 2018 Jun 11.

Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Center for Brain Science, Wako, Saitama, Japan.

Although mitochondrial and serotonergic dysfunctions have been implicated in the etiology of bipolar disorder (BD), the relationship between these unrelated pathways has not been elucidated. A family of BD and chronic progressive external ophthalmoplegia (CPEO) caused by a mutation of the mitochondrial adenine nucleotide translocator 1 (ANT1, SLC25A4) implicated that ANT1 mutations confer a risk of BD. Here, we sequenced ANT1 in 324 probands of NIMH bipolar disorder pedigrees and identified two BD patients carrying heterozygous loss-of-function mutations. Read More

BMC Neurol 2018 May 29;18(1):75. Epub 2018 May 29.

Department of Neurology, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan.

Background: Horizontal gaze palsy with progressive scoliosis (HGPPS) is a rare autosomal recessive congenital anomaly characterized by horizontal gaze limitation and progressive scoliosis. We investigated the underlying pathogenesis by incorporating diffusion tensor imaging and an electrophysiological study.

Case Presentation: A 55-year-old female patient presented to our clinic due to a chronic history of eye movement limitation since childhood. Read More

Can J Cardiol 2018 05 13;34(5):690.e1-690.e3. Epub 2018 Feb 13.

San Fernando General Hospital, San Fernando, Trinidad, West Indies. Electronic address:

Mitochondrial diseases are complex and rare clinical entities that can sometimes be diagnosed by their constellation of simple clinical signs. We describe a 24-year-old insulin-dependent diabetic women who was diagnosed with complete heart block and required permanent pacemaker implantation. Astute physical examination revealed opthalmoparesis, ptosis, and pigmentary retinopathy consistent with a diagnosis of Kearns-Sayre syndrome. Read More

Int Ophthalmol 2019 Jan 26;39(1):213-217. Epub 2018 Mar 26.

Strabismus Service, First Department of Ophthalmology, National and Kapodistrian University of Athens School of Medicine, 32 Socratous Street, Voula, 16673, Athens, Greece.

Background: To report midterm outcomes of strabismus strategy for management of diplopia in chronic progressive external ophthalmoplegia and specific surgical planning rationale.

Design: Retrospective interventional case series.

Results: Two patients, a 26-year-old male and a 36-year-old female, diagnosed with chronic progressive external ophthalmoplegia presented with blepharoptosis and intermittent diplopia. Read More

Neuromuscul Disord 2018 May 21;28(5):408-413. Epub 2018 Feb 21.

Copenhagen Neuromuscular Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.

Muscle dysfunction in mitochondrial myopathy is predominantly caused by insufficient generation of energy. We hypothesise that structural changes in muscles could also contribute to their pathophysiology. The aims of this study were to determine fat fractions and strength in selected muscles in patients with chronic progressive external ophthalmoplegia (CPEO), and compare progression of muscle fat fraction with age in individuals with CPEO vs. Read More

Clin Chim Acta 2018 Jun 10;481:156-160. Epub 2018 Mar 10.

Division of Metabolism and Research Unit of Metabolic Biochemistry, Bambino Gesù Children's Hospital, IRCCS (Institute for Treatment and Research), Viale di S. Paolo 15, 00146 Rome, Italy.

Single large-scale mitochondrial DNA deletions disorders are classified into three main phenotypes with frequent clinical overlap: Pearson marrow-pancreas syndrome (PMS), Kearns-Sayre syndrome (KSS) and chronic progressive external ophtalmoplegia (PEO). So far, only few anecdotal studies have reported on the urinary organic acids profile in this disease class. In this single-center retrospective study, we performed quantitative evaluation of urinary organic acids in a series of 15 pediatric patients, 7 with PMS and 8 with KSS. Read More

Pediatr Med Chir 2017 Dec 15;39(4):169. Epub 2017 Dec 15.

Department of Neurosciences, Ophthalmology, Rehabilitation, Genetics, and Mother-Child Sciences, University of Genoa, Genoa.

The Authors report on a patient with Kearns-Sayre syndrome, large mtDNA deletion (7/kb), facial abnormalities and severe central nervous system (CNS) white matter radiological features, commonly attributed to spongy alterations. The common origin from neural crest cell (NCC) of facial structures (cartilagineous, osseous, vascular and of the peripheral nervous system) and of peripheral glia and partially of the CNS white matter are underlined and the facial and glial abnormalities are attributed to the abnormal reproduction/migration of NCC. In this view, the CNS spongy alterations in KSS may be not only a dystrophic process (leukodystrophy) but also a dysplastic condition (leukodysplasia). Read More

Klin Monbl Augenheilkd 2018 Feb 15;235(2):157-162. Epub 2018 Feb 15.

Augenheilkunde, Universität Basel, Schweiz.

Mitochondrial function is closely linked to numerous aspects of eye health. Imbalance between the creation of energy and the development of reactive oxygen species (ROS) seems to be the cause of the development of mitochondrial dysfunctions. As a result of this energy deficit, the level of oxidative stress in the eye tissues increases, leading to numerous ophthalmic impairments. Read More

Saudi J Anaesth 2018 Jan-Mar;12(1):134-138

Department of Anesthesiology, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia.

Kearns-Sayre syndrome (KSS), a rare form of mitochondrial myopathy, is a triad of chronic progressive external ophthalmoplegia, bilateral pigmentary retinopathy, and cardiac conduction abnormalities. In this report, we show how a combined spinal epidural anesthesia can be useful for cesarean delivery, as we illustrate in a dual-chamber and VVI implantable defibrillator pacemaker/defibrillator parturient with a KSS and preeclampsia. Read More

Neuromuscul Disord 2018 Apr 23;28(4):350-360. Epub 2017 Nov 23.

FMUC - Faculty of Medicine, University of Coimbra, Coimbra, Portugal; CNC - Center for Neuroscience and Cell Biology, Laboratory of Biochemical Genetics, University of Coimbra, Coimbra, Portugal. Electronic address:

Chronic Progressive External Ophthalmoplegia (CPEO) is characterized by ptosis and ophthalmoplegia and is usually caused by mitochondrial DNA (mtDNA) deletions or mt-tRNA mutations. The aim of the present work was to clarify the genetic defect in a patient presenting with CPEO and elucidate the underlying pathogenic mechanism. This 62-year-old female first developed ptosis of the right eye at the age of 12 and subsequently the left eye at 45 years, and was found to have external ophthalmoplegia at the age of 55 years. Read More

Klin Monbl Augenheilkd 2018 Jan 26;235(1):31-33. Epub 2018 Jan 26.

Ophthalmoplastische Chirurgie, Augenlidklinik, München.

Ptosis is often the first symptom of chronic progressive external ophthalmoplegia (CPEO), a rare muscle disorder. As the disease progresses, it can lead to ocular motility defects. Ptosis is present in the early stages of the disease and can be corrected by levator surgery. Read More

Orbit 2018 Oct 15;37(5):385-388. Epub 2018 Jan 15.

a Birmingham Midland Eye Centre , Sandwell and West Birmingham Hospitals NHS Trust , Birmingham , UK.

Methods: We present a rare case with atypical presenting features of unilateral CPEO with a false positive Acetylcholine Receptor Antibody (AchRA) test resulting in diagnostic delay. We illustrate the unilateral nature of this case and demonstrate the caveats of performing myogenic ptosis correction in such patients. We also discuss the differential diagnosis of false positive AchRA, a test commonly performed in the investigation of ptosis. Read More

Medicine (Baltimore) 2017 Dec;96(48):e8869

Department of Neurology, Affiliated Hospital of Jining Medical College, Jining, Shandong, People's Republic of China.

Rationale: Chronic progressive external ophthalmoplegia (CPEO) is a classical mitochondrial ocular disorder characterized by bilateral progressive ptosis and ophthalmoplegia. Kearns -Sayre syndrome (KSS) is a multisystem disorder with PEO, cardiac conduction block, and pigmentary retinopathy. A few individuals with CPEO have other manifestations of KSS, but do not meet all the clinical diagnosis criteria, and this is called "CPEO plus. Read More

Orbit 2018 Oct 4;37(5):371-374. Epub 2018 Jan 4.

a Department of Oculoplastics and Orbital Surgery, Bristol Eye Hospital , Bristol , UK.

Intracranial hypotension (ICH) is characterized by low cerebrospinal fluid pressure, postural headaches, and diffuse pachymeningeal enhancement on magnetic resonance imaging (MRI). A variety of ophthalmoparetic manifestations have been reported in the context of the ICH. The authors describe an unusual case of a 64-year-old woman who presented with rapid onset of headaches, bilateral upper-lid ptosis, and blurring of vision within 4 days after sustaining a trivial head injury. Read More

Mol Cell 2018 01 28;69(1):9-23.e6. Epub 2017 Dec 28.

Department of Medical Biochemistry and Cell Biology, University of Gothenburg, P.O. Box 440, 405 30 Gothenburg, Sweden. Electronic address:

How mtDNA replication is terminated and the newly formed genomes are separated remain unknown. We here demonstrate that the mitochondrial isoform of topoisomerase 3α (Top3α) fulfills this function, acting independently of its nuclear role as a component of the Holliday junction-resolving BLM-Top3α-RMI1-RMI2 (BTR) complex. Our data indicate that mtDNA replication termination occurs via a hemicatenane formed at the origin of H-strand replication and that Top3α is essential for resolving this structure. Read More

Clin Neurol Neurosurg 2018 01 9;164:182-189. Epub 2017 Dec 9.

Dept. of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India; Neuromuscular lab-Neurobiology Research Centre, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. Electronic address:

Objectives: Studies exploring the outcome of epilepsy in patients with mitochondrial disorders are limited. This study examined the outcome of epilepsy in patients with mitochondrial disorders and its relation with the clinical phenotype, genotype and magnetic resonance imaging findings.

Patients And Methods: The cohort was derived from the database of 67 patients with definite genetic diagnosis of mitochondrial disorders evaluated over a period of 11years (2006-2016). Read More

Mitochondrion 2019 01 12;44:15-19. Epub 2017 Dec 12.

McMaster University Medical Centre, Hamilton, ON, Canada. Electronic address:

Chronic progressive external ophthalmoplegia (CPEO) is a common mitochondrial disease. We evaluated the impact of sex and smoking status upon knee extension strength and the phenotypic spectrum of disease in a large cohort of adult-onset CPEO patients (N=116) using retrospective chart analysis. The CPEO patients showed significantly lower knee extension strength as compared to the age- and sex-matched control population (-37%, P<0. Read More

Neuropediatrics 2018 Aug 14;49(4):231-237. Epub 2017 Dec 14.

University of Tunis El Manar and Genomics Platform, Pasteur Institute of Tunis, Tunisia.

Objectives:  Genotype and phenotype of mutation have become increasingly heterogeneous. This review aims at summarizing recent advances concerning the genotypic and phenotypic variability of mutations.

Method:  The review evaluated clinical and instrumental data of 82 patients carrying a mutation in the gene reported in 18 publications with regard to onset, frequency, and type of clinical manifestations and genetic findings. Read More

Brain 2018 01;141(1):e4

Dino Ferrari Centre, Neuroscience Section, Department of Pathophysiology and Transplantation (DEPT), University of Milan, Neurology Unit, IRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy.

Brain 2018 01;141(1):e3

IRCCS Institute of Neurological Sciences of Bologna, Bellaria Hospital, Bologna, Italy.

Nephron 2018 30;138(3):243-248. Epub 2017 Nov 30.

Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Focal segmental glomerulosclerosis (FSGS) is caused by various etiologies, with mitochondrial dysfunction being one of the causes. FSGS is known to be associated with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS), which is a subclass of mitochondrial disease. However, it has rarely been reported in other mitochondrial disease subclasses. Read More

J Pediatr Ophthalmol Strabismus 2017 Nov 17;54:e83-e87. Epub 2017 Nov 17.

The authors describe three examples of "pulled in two syndrome" (PITS) from a series of 13 patients undergoing strabismus surgery with underlying chronic progressive external ophthalmoplegia (CPEO) and illustrate techniques for recovery of the "pulled in two" extraocular muscle should the complication arise. In all cases, a rectus muscle snapped under minimal tension while held on a strabismus hook during strabismus surgery. Two patients suffered from CPEO as a result of genetic mitochondrial disease, whereas one resulted from presumed mitochondrial toxicity induced by HAART. Read More

Andrologia 2017 12;49(10)

Genomics Platform, Pasteur Institute of Tunis, Tunis, Tunisia.

Biol Psychiatry 2018 05 21;83(9):731-738. Epub 2017 Sep 21.

Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan. Electronic address:

Variants in mitochondrial DNA (mtDNA) and nuclear genes encoding mitochondrial proteins in bipolar disorder, depression, or other psychiatric disorders have been studied for decades, since mitochondrial dysfunction was first suggested in the brains of patients with these diseases. Candidate gene association studies initially resulted in findings compatible with the mitochondrial dysfunction hypothesis. Many of those studies, however, were conducted with modest sample sizes (N < 1000), which could cause false positive findings. Read More

Mitochondrion 2018 09 18;42:1-10. Epub 2017 Oct 18.

Department of Neurology, Friedrich-Baur Institute, Ludwig-Maximilians-Universität München, Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Electronic address:

Objectives: To summarise and discuss recent findings and future perspectives concerning mitochondrial disorders (MIDs) affecting the retinal ganglion cells and the optic nerve (mitochondrial optic neuropathy. MON).

Method: Literature review. Read More

Orbit 2018 Jun 20;37(3):201-207. Epub 2017 Oct 20.

a Department of Oculoplastics and Orbit , Athens Eye Hospital , Glyfada , Greece.

Purpose: To present the management of three patients suffering from ptosis of various etiologies, with scleral contact lenses.

Material And Methods: Three patients (five eyes) with ptosis resulting from levator dehiscence due to long-term rigid gas permeable contact lens wear for keratoconus, phthisis bulbi, and myopathy due to Kearns-Sayre syndrome were identified during a 2-year period. They were fitted with scleral contact lenses in order to provide cosmesis by lifting the upper eyelid with the bulk of the lens, and simultaneously provide vision correction where applicable. Read More

BMC Musculoskelet Disord 2017 Oct 19;18(1):419. Epub 2017 Oct 19.

Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Background: Pure exercise intolerance associated with exclusive affection of skeletal muscle is a very rare phenotype of patients with mitochondrial myopathy. Moreover, the exercise intolerance in these rare patients is yet not well explored, as most of known cases have not been assessed by objective testing, but only by interview. We report a patient with a mitochondrial DNA (mtDNA) mutation that gives rise to an exclusive myopathy associated with exercise intolerance and ophthalmoplegia. Read More

Taiwan J Ophthalmol 2017 Jul-Sep;7(3):143-148

Department of Orbit, Oculoplasty, Reconstructive and Aesthetic Services, Sankara Nethralaya Medical Research Foundation, Chennai, Tamil Nadu, India.

Purpose: The purpose of the study was to evaluate the efficacy of silicone rods as frontalis sling for correction of ptosis associated with poor Bell's phenomenon in specific situations.

Materials And Methods: A retrospective interventional case series of 25 eyes of 19 patients who underwent frontalis suspension surgery with silicone rods for ptosis correction from May 2006 to April 2011, was performed. Inclusion criteria included severe ptosis with poor Bell's phenomenon. Read More

Clin Neurophysiol 2017 10 31;128(10):2098. Epub 2017 Jul 31.

Fondation Ophtalmologique A. de Rothschild, Department of Neurology, 25 Rue Manin, Paris, France.