Imaging of the Pes Cavus Deformity

2021 ◽  
Vol 38 (3) ◽  
pp. 303-321
Author(s):  
Lawrence Osher ◽  
Jeffrey E. Shook
Keyword(s):  
Pes Cavus

Randomized trial of botulinum toxin to prevent pes cavus progression in pediatric charcot-marie-tooth disease type 1A

2010 ◽  
Vol 42 (2) ◽  
pp. 262-267 ◽  
Author(s):  
Joshua Burns ◽  
Adam Scheinberg ◽  
Monique M. Ryan ◽  
Kristy J. Rose ◽  
Robert A. Ouvrier
Keyword(s):  
Botulinum Toxin ◽  
Randomized Trial ◽  
Disease Type ◽  
Pes Cavus ◽  
Charcot Marie Tooth ◽  
Charcot Marie Tooth Disease ◽  
Tooth Disease

Idiopathic pes cavus in adults is not associated with neurophysiological impairment in the lower limbs

2015 ◽  
Vol 36 (12) ◽  
pp. 2287-2290 ◽  
Author(s):  
Roberto Di Fabio ◽  
Ludovico Lispi ◽  
Filippo Maria Santorelli ◽  
Claudio Castagnoli ◽  
Andrea Matrigale ◽  
...  
Keyword(s):  
Lower Limbs ◽  
Pes Cavus

Influence of running shoe type on distribution and magnitude of plantar pressures among those with pes planus or pes cavus feet

2008 ◽  
Vol 23 (5) ◽  
pp. 708-709 ◽  
Author(s):  
Joseph M. Molloy ◽  
Nancy S. Yeykal ◽  
Bradley S. Tragord ◽  
Matthew S. Neal ◽  
Eric S. Nelson ◽  
...  
Keyword(s):  
Pes Cavus ◽  
Pes Planus ◽  
Plantar Pressures

THE PES CAVUS OF CONGENITAL SYPHILIS

JAMA ◽  
1926 ◽  
Vol 86 (6) ◽  
pp. 392 ◽  
Author(s):  
C. W. GOFF
Keyword(s):  
Congenital Syphilis ◽  
Pes Cavus

scholarly journals ATP1A3-Related Disorders: An Ever-Expanding Clinical Spectrum

2021 ◽  
Vol 12 ◽  
Author(s):  
Philippe A. Salles ◽  
Ignacio F. Mata ◽  
Tobias Brünger ◽  
Dennis Lal ◽  
Hubert H. Fernandez
Keyword(s):  
Original Description ◽  
Rapid Onset ◽  
Acute Onset ◽  
Clinical Spectrum ◽  
Pes Cavus ◽  
Sodium Potassium ◽  
Pathogenic Variants ◽  
Alternating Hemiplegia Of Childhood ◽  
The Central Nervous System ◽  
Neurological Features

The Na+/K+ ATPases are Sodium-Potassium exchanging pumps, with a heteromeric α-β-γ protein complex. The α3 isoform is required as a rescue pump, after repeated action potentials, with a distribution predominantly in neurons of the central nervous system. This isoform is encoded by the ATP1A3 gene. Pathogenic variants in this gene have been implicated in several phenotypes in the last decades. Carriers of pathogenic variants in this gene manifest neurological and non-neurological features in many combinations, usually with an acute onset and paroxysmal episodes triggered by fever or other factors. The first three syndromes described were: (1) rapid-onset dystonia parkinsonism; (2) alternating hemiplegia of childhood; and, (3) cerebellar ataxia, pes cavus, optic atrophy, and sensorineural hearing loss (CAPOS syndrome). Since their original description, an expanding number of cases presenting with atypical and overlapping features have been reported. Because of this, ATP1A3-disorders are now beginning to be viewed as a phenotypic continuum representing discrete expressions along a broadly heterogeneous clinical spectrum.

scholarly journals Genetics of Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS) and Role of Sacsin in Neurodegeneration

2022 ◽  
Vol 23 (1) ◽  
pp. 552
Author(s):  
Jaya Bagaria ◽  
Eva Bagyinszky ◽  
Seong Soo A. An
Keyword(s):  
Neurodegenerative Diseases ◽  
Autosomal Recessive ◽  
Genetic Mutations ◽  
Compound Heterozygous ◽  
French Canadians ◽  
Pes Cavus ◽  
Spastic Ataxia ◽  
Mitochondrial Functions ◽  
Limb Deformities

Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is an early-onset neurodegenerative disease that was originally discovered in the population from the Charlevoix-Saguenay-Lac-Saint-Jean (CSLSJ) region in Quebec. Although the disease progression of ARSACS may start in early childhood, cases with later onset have also been observed. Spasticity and ataxia could be common phenotypes, and retinal optic nerve hypermyelination is detected in the majority of patients. Other symptoms, such as pes cavus, ataxia and limb deformities, are also frequently observed in affected individuals. More than 200 mutations have been discovered in the SACS gene around the world. Besides French Canadians, SACS genetics have been extensively studied in Tunisia or Japan. Recently, emerging studies discovered SACS mutations in several other countries. SACS mutations could be associated with pathogenicity either in the homozygous or compound heterozygous stages. Sacsin has been confirmed to be involved in chaperon activities, controlling the microtubule balance or cell migration. Additionally, sacsin may also play a crucial role in regulating the mitochondrial functions. Through these mechanisms, it may share common mechanisms with other neurodegenerative diseases. Further studies are needed to define the exact functions of sacsin. This review introduces the genetic mutations discovered in the SACS gene and discusses its pathomechanisms and its possible involvement in other neurodegenerative diseases.

scholarly journals Pes cavus

2012 ◽  
Author(s):  
Jeremy Jones ◽  
Yuranga Weerakkody
Keyword(s):  
Pes Cavus

Quantification of Muscle Strength and Imbalance in Neurogenic Pes Cavus, Compared to Health Controls, Using Hand-Held Dynamometry

2005 ◽  
Vol 26 (7) ◽  
pp. 540-544 ◽  
Author(s):  
Joshua Burns ◽  
Anthony Redmond ◽  
Robert Ouvrier ◽  
Jack Crosbie
Keyword(s):  
Muscle Strength ◽  
Healthy Controls ◽  
Foot And Ankle ◽  
Foot Deformity ◽  
Pes Cavus ◽  
Retest Reliability ◽  
Ankle Muscle ◽  
Cavus Foot ◽  
Muscle Groups ◽  
Test Retest Reliability

Background: Pes cavus foot deformity in neuromuscular disease is thought to be related to an imbalance of musculature around the foot and ankle. The most common cause of neurogenic pes cavus is Charcot-Marie-Tooth (CMT) disease. The aim of this investigation was to objectively quantify muscle strength and imbalance using hand-held dynamometry in patients diagnosed with CMT and pes cavus, compared to healthy controls. Methods: Muscles responsible for inversion, eversion, plantarflexion, and dorsiflexion of the foot and ankle were measured in 55 subjects (11 CMT patients with a frank pes cavus, and 44 healthy controls with normal feet) using the Nicholas hand-held dynamometer (HHD). Test-retest reliability of the HHD procedure also was determined for each of the four muscle groups in the healthy controls. Results: Test-retest reliability of the HHD procedure was excellent (ICC3,1 = 0.88 to 0.95) and the measurement error was low (SEM = 0.3 to 0.7 kg). Patients with CMT were significantly weaker than normal for all foot and ankle muscle groups tested ( p <0.001). Strength ratios of inversion-to-eversion and plantarflexion-to-dorsiflexion were significantly higher in the patients with CMT and pes cavus compared to individuals with normal foot types ( p > 0.01). Conclusions: Hand-held dynamometry is an objective and reliable instrument to measure muscle strength and imbalance in patients with CMT and a pes cavus foot deformity.

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