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PubMedDate not supplied

Teratogenic mechanisms of longitudinal deficiency and cleft hand.

In order to better understand the teratogenic mechanisms of congenital defects of the digits, we analyzed clinical cases and induced similar types of congenital hand anomalies in rat fetuses by oral administration of busulfan. In clinical cases, radial and ulnar deficiencies had common characteristic features. We induced radial and ulnar deficiencies in rat fetuses with the same drug. Radial and ulnar deficiencies induced in rats have similar clinical manifestations and these anomalies might be caused by the same teratogenic mechanism. Then, the formation of the digital rays was examined histologically. The results of histological examination suggested that these deficiencies were not caused by localized damage of the limb bud. They also suggested that the cause of missing digits in longitudinal deficiency is closely related to a deficit of mesenchymal cells in the limb bud. Cleft hand is considered to be one of the types of longitudinal deficiency. However, several investigators have suggested that the abnormal induction of finger rays in the process of formation of fingers induced central polydactyly, osseous syndactyly and also cleft hand. X-rays of the clinical cases and skeletal changes of the anomalies induced in rats appear to demonstrate that cleft hand formation proceeds from osseous syndactyly and central polydactyly. The results of our experimental study show that the critical periods of central polydactyly, osseous syndactyly and cleft hand are the same. They also suggest that central polydactyly, syndactyly and cleft hand might be induced when the same teratogenic factor acts on embryos at the same developmental stage in the human being. Because they have a similar causation, cleft hand, syndactyly and central polydactyly should be classified into the same entity, that is, abnormal induction of digital rays. Based on these clinical and experimental studies, we modified the Swanson classification. In our modified classification, typical cleft hand, syndactyly and polydactyly are included in the same category of abnormal induction of digital rays as the fourth new category.

Animals↗
PubMed2003

Treatment of the hands and feet in Apert syndrome: an evolution in management.

Apert syndrome is a relatively uncommon condition that is instantly recognizable on the basis of the pan-syndactylies involving both the hands and feet. For more than 10 years, the treatment of Apert syndrome hand and foot anomalies was approached in a comprehensive manner, with attempts to maximize the final results and minimize the total number of operations. Numerous conventions were abandoned in the development of this approach, with the introduction of some new methodologies, including (1) release of all 10 fingers, and toes, in only two operations, (2) elimination of routine digital amputations, (3) abandonment of the zigzag incision in favor of straight-line release, (4) substitution of equal-length anterior and posterior flaps for the long dorsal web space lining flap, (5) leaving of small areas of exposed bone without vascularized tissue coverage, and (6) performance of midphalangeal osteotomies, among older children, to improve hand function. Fifty-seven children with Apert syndrome have been treated at the author's center since 1990, and 43 underwent surgical treatment of their hands and feet by a single surgeon. Treatment can be separated into two phases, early (syndactyly releases) and late (functional osteotomies). Seventeen of those 43 patients were treated at the author's center from birth (type I, 11 patients; type II, two patients; type III, four patients), and 10 fingers and 10 toes were achieved for all patients in two operations. No digital amputations were performed for any of the 43 patients. However, four of 26 patients (15 percent) not treated at the author's center from birth had undergone at least one digital amputation before coming to the center. Twenty-two of those 26 patients required a two-stage syndactyly release to accomplish the separation of all 10 fingers and toes. Aside from the patients who had previously undergone amputations, all other patients successfully achieved 10 fingers and toes, except for one patient (38 of 39 patients, 97 percent). The average operative time for the first-stage syndactyly release of the hands and feet was 4 hours 11 minutes (range, 185 to 300 minutes), and that for the second stage was 3 hours 49 minutes (range, 160 to 300 minutes). Twenty-eight hands were treated with functional osteotomies, which involved permanent angulation of the fused phalanges at the proximal interphalangeal level, to create a "position of function" and provide pulp-to-pulp pinch. In addition, targeted osteotomies of the feet were performed for many of these patients, to decrease pain with walking. There were no major complications. Minor complications included one reexploration because of bleeding, early in the series. There were 13 incomplete secondary syndactylies that required a subsequent operative release (10 spaces treated at the author's center and three treated elsewhere), of a total of 342 spaces (3 percent author incidence). There were no scar contractures or functional limitations that required release. This distinctive protocol seemed to result in improved functional outcomes, with a reduction in the total number of operative procedures.

Acrocephalosyndactylia↗
PubMed2000

[Complex and complicated syndactylia. Review and treatment progress].

Complex syndactyly is generally defined as abnormal digital interconnection by bone, but sometimes simple syndactyly with complicated cutaneous, musculotendinous or neurovascular interconnections should be considered complex as well. Additionally, complex syndactyly involving anomalous bones (delta phalanx, brachiphalangism...) falls in different category called "complicated". 35 patients with complex or complicated congenital syndactyly are studied and 58 children with cutaneous syndactyly due to burns and epidermolysis bullosa are analyzed as well.

Child↗
PubMed1991

The prevalence at birth of cogenital malformations at a maternity hospital in Osaka City, 1948-1990.

The frequencies of congenital malformations at St. Barnabas' Hospital, Osaka were studied during the period 1948-1990. There were 1,418 malformed infants diagnosed during the first week of life among a total number of 131,996 births during the period. Of the 1.07% of malformed children, 0.90% had single and 0.17% had multiple malformations. The birth prevalence was 1.07% in singletons and 1.20% in twins. There was significant difference in prevalence between males (1.15%) and females (0.97%). The prevalence was 0.88% for the period 1948-1958 and increased with each year cohort up to the recent period when the value was 1.38%. Varus deformities of feet was the most common defect (23.4 per 10,000 births), followed by polydactyly (finger) (7.8), anencephaly (7.1), cleft lip and palate (6.5), syndactyly (toe) (6.5), cleft lip (6.3), and Down's syndrome (6.1). The prevalence of conjoined twins was 1 in 65,551 deliveries. Significant differences occurred between males and females for cleft palate, cleft lip and palate, syndactyly (finger), oligodactyly (finger), and hypoplastic auricle. The prevalences for valgus deformities of feet, syndactyly (toe) and atresia ani increased significantly with the year cohort, whereas the prevalence of cleft palate decreased significantly with the year cohort. Overall prevalence was significantly higher in 1970-1990 (1.28% than in 1948-1969 (0.88%). Similar results were examined for cleft lip and palate, syndactyly (finger), syndactyly (toe), hypospadias, hydrocele testis, and Down's syndrome.

Congenital Abnormalities↗
PubMed2005

Molecular analysis of non-syndromic preaxial polydactyly: preaxial polydactyly type-IV and preaxial polydactyly type-I.

Human GLI3 gene mutations have been identified in several phenotypes of digital abnormality such as Greig cephalopolysyndactyly syndrome, Pallister-Hall syndrome, preaxial polydactyly type-IV (PPD-IV) and postaxial polydactyly. However, the different phenotypes resulting from GLI3 mutations have not yet been properly defined. We have experienced two types of digital abnormality without other complicating developmental defects; a family with foot PPD-IV with syndactyly of the third and fourth fingers, and four sporadic cases with biphalangeal thumb polydactyly (PPD-I). The genes responsible for syndactyly of the third and fourth fingers (syndactyly type-I) and PPD-I have not yet been identified; we therefore examined the involvement of the GLI3 gene in these subtypes of digital abnormality. We found a non-sense mutation in the GLI3 gene in the family with foot PPD-IV accompanied with hand syndactyly of the third and fourth fingers, but no mutations were detected in the GLI3 gene in the four other cases with PPD-I alone. Thus, the phenotype of foot PPD-IV accompanied with hand syndactyly of the third and fourth fingers may result from a GLI3 mutation, whereas the PPD-I phenotype alone is not caused by GLI3 gene defect. These results will help to define the phenotypic spectrum of GLI3 morphopathies, which have been recently proposed.

Codon, Nonsense↗
PubMed2005

[HOXD13 polyalanine tract expansion in synpolydactyly: mutation detection and prenatal diagnosis in a large Chinese family].

OBJECTIVE: Synpolydactyly (SPD, MIM 186000), also known as syndactyly type II, is a dominantly inherited limb malformation with incomplete penetrance and variable expressivity. Polyalanine tract expansion in HOXD13 has been shown to be the disease-causing mutation in SPD. The present study was designed to identify mutation in HOXD13 and to provide prenatal diagnosis, in a large Chinese SPD family consisting of 54 individuals. METHODS: The proband and 4 other affected individuals in the family were evaluated physically and radiologically to ascertain the SPD phenotype. Genomic DNA was extracted from peripheral blood samples obtained from 18 family members (9 affected and 9 unaffected), and from amniotic fluid and chorionic villus samples obtained from the proband during her two consecutive pregnancies. With the use of a pair of specific primers, a fragment of 161bp was amplified by polymerase chain reaction (PCR) to cover the imperfect GCN triplet repeat sequence in exon 1 of HOXD13 encoding the 15-residue polyalanine tract. The PCR products were detected by agarose gel electrophoresis, and sequenced after cloning into pMD18T vector. To confirm prenatal diagnosis, haplotype analysis was also performed by allele-typing three microsatellite markers, including the intronic CA repeats in HOXD13. RESULTS: Digital and radiographic findings indicated a typical SPD phenotype in the family. These included 3/4 finger syndactyly and 4/5 toe syndactyly with an extra digit in the syndactylous web. Unilateral finger syndactyly in the proband, unilateral toe syndactyly in 2 individuals, bilateral brachydactyly of the fifth toes in 1 individual, and clinodactyly of the fifth fingers in 4 individuals were also observed, indicating variable expressivity. Gel electrophoresis of the PCR products showed an additional longer fragment in all 9 affected individuals but not in the unaffected ones. Sequence analysis of the longer fragment revealed a 9-alanine expansion. The expansion was detectable in DNA from the amniotic fluid and chorionic villus samples. Furthermore, haplotype analysis ruled out potential contamination of the maternal DNA. These suggested that the two fetuses carried the same polyalanine expansion. CONCLUSION: HOXD13 polyalanine expansion was detected in a large Chinese family with SPD and prenatal diagnosis of two affected fetuses was achieved. This is the first report on prenatal diagnosis of SPD by detecting the HOXD13 polyalanine expansion in the Han population of the Chinese mainland.

Base Sequence↗
PubMed2003

[Genetic analysis of a Chinese pedigree with congenital synpolydactyly].

Syndactyly is a limb malformation that shows a characteristic manifestation in both hands and feet. This condition is inherited as an autosomal dominant trait with reduced penetrance. Clinical presentation, in general, is complete or partial webbing between 3rd and 4th fingers. Syndactyly type I, II and III were mapped to 2q34-36, 2q31-q32 and 6q21-23.2 respectively. Syndactyly type II is named as synpolydactyly (SPD). Expansion of a polyalanine tract in the HOXD13 gene is known to cause synpolydactyly. HOXD13 gene locates in the HoxD complex. Nine homologous genes (HOXD1, -D3, -D4, -D8, -D9, -D10, -D11, -D12, -D13) of HoxD complex locate on chromosome 2 in the order of HOXD1 to HOXD13, among which HOXD13 is closest to the centromere. Deletions and duplications in HoxD complex or its upstream regulator factors have been identified to cause hand heteroplasia and consequently lead to abnormity of finger number or abnormity of configuration. We performed linkage analysis in a kindred with autosomal dominant hereditary syndactyly. Tight linkage to markers on chromosome 2q31-q32 (maximum two-point lod score: 6.78 at recombination fraction theta = 0.00) was observed. Multipoint linkage analysis produced a maximum LOD score of 7.02. Haplotype construction and analysis of recombination events narrowed this locus to a 20.61 cM region between markers D2S2302 and D2S315. No mutation was found in the coding region, the intro-exon boundaries, or part of the promoter region of HOXD13. Our result demonstrates that synpolydactyly locus in the Chinese Han Population is in the region of chromosome 2q31-q32 but a different causal gene can be involved.

China↗
PubMed1990

Cleft hand.

Definition, incidence, genetics, and etiology of typical cleft hand are discussed in this paper. Cleft hand, central polydactyly, and osseous syndactyly were induced experimentally when the same teratogenic factors acted on the embryos at the same developmental stage. Typical cleft hand, central polydactyly, and syndactyly should be classified together as manifestations of the same entity, that is, failure of induction of finger rays. Typical cleft hand may be further subdivided into five types on the basis of the number of defective finger rays. Treatment of the typical cleft hand involves cosmetic and functional considerations. Reduction of the wide interdigital space is performed primarily for cosmetic reasons, while separation of syndactyly between thumb and index finger and correction of deviation of the thumb is performed for functional improvement. A zigzag incision with a small triangular flap is recommended for reduction of the interdigital space. If metacarpal remnants or cross bones prevent drawing the metacarpals together, they should be removed. The deep transverse metacarpal ligament should be reconstructed by ligamentous flap made out of the flexor tendon sheaths of the index and ring fingers to prevent later spreading of the fingers. A dorsal-based rotation flap fashioned from the skin of the cleft is recommended for the treatment of cleft hand with partial syndactyly of the thumb and index finger. Deviation of the thumb is often caused by a delta phalanx by a trapezoidal-shaped extra phalanx. Deviation of the thumb is corrected by removing the delta phalanx or osteotomy of the trapezoidal phalanx. When the cleft is closed at approximately 1 year of age, spontaneous correction of the flexion deformity of the ring finger is sometimes observed.

Hand Deformities, Congenital↗
PubMed1984

[Syndactylia results].

During the years 1960-1980 42 patients with syndactyly were treated at the Department for Handsurgery of the University of Munich. In addition to the conventional classification and in regard to the criteria for operative management, we stress the difference between the simple and the more complex forms of syndactyly as well as those cases in which the syndactyly is part of a syndrome. There was a relation of 1:1 between the simple and the 'complex' syndactyly. The results of former and modern operative management are reviewed and the value of some special methods is pointed out.

Adolescent↗
PubMed1993

[The treatment of syndactylia and results in 31 children].

In recent years there have been some changes in the treatment of congenital syndactyly. Nowadays treatment is started in the first year of life, before the child uses his hands purposefully. In the University Hospital of the Free University of Amsterdam 31 patients with 61 congenital syndactylies in 45 hands were treated between 1971 and 1991. The results were good in 40, fair in 15, moderate in 4 and poor in 2 corrections. Surgery was performed under general anaesthesia and whenever possible on an out-patient basis. To split the fingers zig-zag incisions are used. For web reconstruction two triangular flaps or one rectangular flap are used. Complex syndactyly is treated in two sessions: first two double opposing palmar flaps to cover the tips and to form the nail walls are raised and after two weeks the rest of the syndactyly is corrected. Postoperative treatment consists of a compression bandage for two weeks, followed by bathing and training in warm water until all wounds have healed.

Adolescent↗
PubMed1998

Analysis of interdigital spaces during mouse limb development at intervals following amniotic sac puncture.

A spectrum of limb abnormalities ranging from adactyly, syndactyly, acrosyndactyly to nail hypoplasia was encountered in mouse embryos subjected to amniotic sac puncture at the corresponding gestational stage when human chorionic villus sampling (cvs) would normally be performed clinically. Previous skeletal studies revealed that, apart from the occasional incidence of fusion of 2 distal phalanges, syndactyly usually only affected the soft tissues within the interdigital spaces. A similar situation was also observed in cases of adactyly; while the skeletal elements of the digits were present, the soft tissues in the interdigital spaces failed to separate. A transient period of bradycardia is induced, possibly secondary to compression of the embryo by the extraembryonic membranes and uterine muscles following amniotic sac puncture. These factors, we believe, produce temporary hypoxia/ischaemia of the distal extremities, and may lead to the modification of the interdigital mesenchymal tissues within the autopods. In order to investigate the mechanism(s) underlying soft tissue syndactyly, limbs recovered at 0.5, 4, 8, 12, 24, or 36 h following amniotic sac puncture (ASP) were examined histologically. Vascular disruption in the form of localised areas of haemorrhage, vascular dilatation and congestion and the presence of fluid-filled cavities occurred in relation to the marginal vein and vascular plexus in the interdigital spaces. It is hypothesised that this interfered with the normal equilibrium of the preset programs of mitosis/cell death and apoptosis within the mesenchymal cells of the interdigital spaces. Apoptosis in these areas was inhibited in the majority of the experimental limbs analysed 4 h after ASP. Instead of undergoing necrosis/apoptosis, increased mitotic activity was usually observed from 8 h following ASP at the sites where apoptosis would normally be expected to be seen. The aberrant fate of the interdigital mesenchyme following ASP and the underlying mechanism(s) involved are discussed, as is the critical importance of an adequate vascular supply to the interdigital spaces during the morphogenesis of the autopod. We believe that this report contributes to understanding the mechanism(s) which lead to syndactyly following ASP, and the limb defects occasionally seen following cvs when this is undertaken during early gestation.

Animals↗
PubMed1987

Triphalangeal thumb and brachy-ectrodactyly syndrome. Confirmation of autosomal dominant inheritance.

Two patients with triphalangeal thumbs-ectrodactyly syndrome are described. The first case is a 4-year-old female with triphalangeal thumbs, preaxial polydactyly with rudimentary polydactyly of the 3rd finger of the right hand and ectro-syndactyly of feet. Her stillborn sister had triphalangeal thumbs and ectrodactyly of feet. The mother has triphalangeal thumbs, brachy-syndactyly of the left foot and ectro-syndactyly of the right one. The maternal grandmother has syndactyly of 1st, 2nd, 3rd toes and hypoplasia of the 3rd toe on the right foot. The second case is sporadic and shows triphalangeal thumbs, preaxial polydactyly of the right hand and bilateral lobster-claw feet. Our observations confirm the variability of clinical expression and support the autosomal dominant inheritance of the syndrome.

Abnormalities, Multiple↗
PubMed1993

Synaptic mechanisms of cortical representational plasticity: somatosensory and corticocortical EPSPs in reorganized raccoon SI cortex.

1. Reorganizations of representational maps have been described for a variety of sensory and motor regions of cerebral neocortex in several species. The purpose of this study was to investigate synaptic mechanisms of the reorganizations of primary somatosensory cortex that follow removal of a digit or the joining of two digits into a syndactyly. We examined neurons in the cortical representation of digit 4 (d4). Intracellular recording was used to compare somatosensory and corticocortical excitatory postsynaptic potentials (EPSPs) in normal raccoons, with EPSPs recorded in two experimental groups of animals surviving for a mean of 22 wk after removal of d4, or union of d4 with digit 3 (d3). 2. In normal animals with d4 intact, EPSPs were evoked from this on-focus digit in 100% of cortical neurons. EPSPs were evoked from d3 and digit 5 (off-focus digits) in only a minority of neurons in normal raccoons. The incidence of somatosensory EPSPs from off-focus digits increased dramatically after removal of d4 or its union with d3. Latencies of EPSPs evoked from off-focus digits decreased after d4 removal, so that they were as short as latencies from d4 in normal animals. In contrast, for the group of animals with d3-d4 syndactyly, latencies of EPSPs from off-focus digits were not shorter than responses from these digits in normal animals. 3. Corticocortical EPSPs were no more common in animals with d4 removed than in intact animals. Furthermore, corticocortical EPSPs after d4 removal did not differ in their latencies, amplitudes, half-widths, or integrated amplitudes. The only detected change was that corticocortical EPSPs had faster rising phases after removal of d4. In contrast, after d3-d4 syndactyly, corticocortical EPSPs were more common than in normal animals. 4. Digit removal and digital syndactyly had distinctive effects on somatosensory and corticocortical EPSPs. These results do not identify unique synaptic mechanisms for cortical representational plasticity, nor do they specify the involved CNS site(s). Several synaptic mechanisms consistent with the results are considered in the DISCUSSION, including synaptic proliferation to form new synaptic connections and enhanced effectiveness of existing corticocortical synapses.

Afferent Pathways↗
PubMed1999

Brachydactyly type B: case report and further evidence for clinical heterogeneity.

We present a male child with digital and radiographic findings consistent with brachydactyly type B. His left hand had 2-4 syndactyly, shortened first and fifth digits and single palmar and fifth finger flexion creases. The nail on the second finger was hypoplastic. The right hand had a small thumb and curving of the second finger towards the midline. The left foot had a short left hallux with an absent nail, 2-4 syndactyly and an absent toe. His right foot had a short, dorsiflexed hallux with a hypoplastic nail, 2-3 syndactyly and an overlapping toe. Radiographs showed asymmetrical hypoplasia of the middle and terminal phalanges and there were no extra-articular findings to suggest Sorsby syndrome. Brachydactyly type B has classically been described as hypoplasia or absence of the terminal phalanges with absent nails. Although other digital anomalies have previously been described with brachydactyly type B, the absent digit, atypical syndactyly and marked asymmetry in this child make this case a good illustration of the clinical heterogeneity that can be associated with this type of brachdactyly. We provide a brief review of syndromes in which similar digital malformations have been reported.

Hand Deformities, Congenital↗
PubMed1991

Pattern of limb malformations in mice induced by methoxyacetic acid.

The present study investigated the pattern of limb malformations induced in mice by methoxyacetic acid (MAA), one of di(2-methoxyethyl) phthalate (DMEP) metabolites. Pregnant Jcl:ICR mice were given orally at gestational day (gd) 10.5, 11.0, or 11.5 (vaginal plug = gd 0) a single dose of MAA 10 mmol/kg of body weight. Fetuses were examined at gd 15.5 for external and skeletal malformations. Limb defects were maximum in frequency and severity after administration at gd 11.5. Forelimbs had greater susceptibility than hindlimbs. Treatment at gd 10.5 produced cutaneous or osseous syndactyly between digits I and II, II and III, and ectrodactyly of digit II or digit I. Intercalary defects in the forelimbs were also detected. No hindlimb malformations were induced. Treatment at gd 11.0 induced ectrodactyly of digit II and digit I in the forelimbs, as well as osseous syndactyly or intercalary defects of the metacarpals or phalanges, and the frequency became increased. Hindlimb malformations were also detected in a small number with syndactyly between digits I and II or ectrodactyly in digit I. Treatment at gd 11.5 induced ectrodactyly in the forelimbs. Half of the forelimbs showed ectrodactyly with four missing digits (digits I, II, III, and V) and the remaining limbs showed ectrodactyly with a similar frequency with one, two, or three missing digits, either in the pre- or postaxial area. In the hindlimbs ectrodactyly with one, two, or three missing digits was the most common malformation observed. Syndactyly between digits I and II was also induced in a small percentage.

Abnormalities, Drug-Induced↗
PubMed1990

The craniodigital syndrome of Scott: report of a second family.

We report on a boy with a characteristic combination of facial anomalies, syndactylies of fingers and toes, and mental retardation. Scott et al. (Journal of Pediatrics 78:658-663, 1971) observed 3 brothers with almost identical manifestations. The mother of these patients had bilateral syndactyly of toes 2 and 3. This led the authors to suggest X-linked inheritance. The mother of our patient also has cutaneous syndactyly between the second and third toes, strengthening the hypothesis of X-linked inheritance.

Face↗
PubMed1994

Familial crossed polysyndactyly.

We have observed a distinct form of "crossed" polysyndactyly in 6 generations of a family with 5 affected persons, all males. The polydactyly is postaxial in the hands and preaxial in the feet. Syndactyly in the hands is observed in some relatives, while syndactyly in the feet is present bilaterally in all affected relatives. This seems to be an autosomal dominant trait with male to male transmission over 3 generations by examination and an additional 3 generations by history. This form of polysyndactyly could not be readily categorized by the existing classification by Temtamy and McKusick [1978: BD OAS XIV 6:363-392]. We review and expand the present classification of polydactyly and syndactyly syndromes.

Abnormalities, Multiple↗
PubMed2004

Cleft hands with six metacarpals.

PURPOSE: The purpose of this study was to identify children with cleft hands whose radiographs showed metacarpal polydactyly with 6 metacarpals to support the hypothesis that cleft hand develops not as a result of a longitudinal failure of formation but through a process of central polydactyly and osseous syndactyly. METHODS: We screened the hand radiographs of all children with a transverse or longitudinal deficiency of the upper limb and identified 8 children with cleft hands containing 6 metacarpals. RESULTS: Six cleft hands had a missing middle finger and consisted of a thumb and index finger separated from the ring and small fingers by a V-shaped central cleft. Two children had a more severe form of cleft hand with absence of both the index and middle fingers but presence of 6 metacarpals. CONCLUSIONS: These 8 cleft hands containing 6 metacarpals showed progression of polydactyly of the middle finger and osseous syndactyly between the 2 middle finger metacarpals and the adjacent index and ring finger metacarpals. This contradicts a longitudinal failure of formation mechanism and supports the alternative hypothesis that cleft hand, polydactyly, and syndactyly develop through a similar teratogenic mechanism. The 2 cleft hands that had more severe suppression of the index and middle fingers yet had 6 metacarpal polydactyly provided confirmatory evidence that both typical cleft hands and the more severe manifestations of cleft hand with absence of multiple digits develop through a similar failure of induction mechanism.

Child↗