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P Mouton

Publications and source records attributed to P Mouton.

At least 19 recordsLinked to original sources
PubMed2006

[The dorsoradial flap: a new flap for hand reconstruction. Anatomical study and clinical applications].

The authors report a new cutaneous flap harvested from the dorsal and distal quarter of the forearm: the dorsoradial flap. The vascularisation type of the cutaneous paddle belongs this flap to the anterograde and axial family flaps. The anatomical study carried out on thirty six fresh cadaver upper arms showed a constant and a consistent cutaneous collateral branch of the radial artery which arises at the apex of the first intermetacarpal space. Two anatomical types were recorded according to the origin of the dorsoradial artery: type I (84% of cases), the vessel arises directly from the radial artery; type II (16% of cases), it arises from a common trunk with the first dorsal intermetacarpal artery. Those anatomical findings does not influence the flap operative technique, the flap design and the location of the pedicle pivot point. The dorsoradial artery emerges vertically from the apex of the first intermetacarpal space, crosses the angle between the extensor pollicis longus tendon laterally and the extensor carpi radialis longus tendon medially and turns proximally towards the distal radio-ulnar joint. Over the dorsal aspect of the wrist, the dorsoradial artery enters the subcutaneous tissue, runs parallel to the extensor pollicis longus tendon at three millimeters in a medial position, passes over the medial collateral branch of the superficial radial nerve and irrigates all the distal and dorsal quarter of the forearm. The artery is consistently accompanied by two comitantes veins, which assume the venous drainage of the cutaneous territory. The flap paddle is designed over the distal dorsal forearm quarter, between the dorsal crease of the wrist distally, the ulnar crest medially and the radial crest laterally. All this skin territory can be harvested and supplied by the dorsoradial pedicle, but we always should deal with the needs of the defects reconstruction and the morbidity of the donor site. The vascular pedicle is outlined between the distal radio-ulnar joint and the apex of the first intermetacarpal space with a minimum of one centimeter width. The surgical procedure is carried out under a tourniquet without an upper arm exsanguination. The skin is firstly dissected over the vascular pedicle through an S shape incision; it is lifted on the dermo-hypodermis plan preserving all the superficial venous network with the pedicle. The flap is elevated from proximal to distal including the dorsal forearm fascia. Over the dorsal extensor retinaculum, the dissection is underwent close to it elevating all the subcutaneous tissues. The medial collateral branch of the superficial radial nerve should be identified and respected. At the distal border of the dorsal retinaculum, the extensor pollicis longus and the extensor carpi radialis longus tendons are identified and retracted. The pedicle dissection goes deeper between this two tendons towards the first web space. It takes all the areolar tissue around the pedicle in order to preserve the venous network of the cutaneous paddle. The donor site is closed primarily if the skin width does not exceed 3 cm or grafted secondarily. Its large rotational arc allows the cutaneous paddle to cover the dorsal hand and metacarpo-phalangeal long fingers defects, the dorsal aspect of the thumb and the first intermetacarpal space. It can also safely reach the palmar aspect of the wrist. We report four clinical cases where the dorsoradial flap was successfully applied. This preliminary clinical experience exhibits the vascular network reliability and the operative technique simplicity of this new cutaneous flap. We believe that it should be added to the armamentarium of the reconstructive hand surgeon and considered as a useful tool for soft tissue hand and thumb reconstruction defects.

Adult↗
PubMed2006

[A 'psychogenic psychosis' turns out to be a subarachnoid haemorrhage. A case study].

A 50-year-old woman is admitted to the emergency ward by reason of her psychotic state. Because she has a history of psychiatric problems and has been previously diagnosed as having borderline personality disorder it is assumed that she has had a brief psychogenic psychosis. When the psychosis recurs and the symptoms increase in intensity the patient is given a computerized tomography brain scan. The scan reveals a subarachnoid haemorrhage. In discussing this case history we try to interpret the symptoms of this neurological disorder against the background of the premorbid psychiatric diagnosis. We supplement our interpretation with data from case histories reported in the literature.

Diagnosis, Differential↗
PubMed2005

[The Omega "Omega" pulley plasty. A new technique to increase the diameter of the annular flexor digital pulleys].

The authors report a new technique of pulley plasty of the flexor digital system. It is not an operative procedure to reconstruct a damaged pulley but an original way to expand the volume of an intact pulley in order to adapt its volume to the diameter of the repaired flexor tendon. The flexor tendons ruptures in Verdan zone II and particularly in Tang zones IIA and IIB are often accompanied by an osteofibrous tunnel injury. Initially, the tendon sheath closure was advised after tendons repair. This sheath recovery had to have an effect on tendons nutrition by establishing the synovial cavity continuity and particularly to protect the tendons from adhesions formation. The closure of the digital tube was rapidly shown to be unnecessary creating an obstacle to the tendons movements without any effect on tendons healing. In primary tendon management, the tendon repair is associated with an increase of the tendon diameter. An incongruence appears with the surrounding digital tube with gliding resistance complicating the tendon injury recovery. In secondary tendon injury management, the flexor digital tube is subject to healing and inflammatory process. This situation with the absence of the flexor tendon generates a retraction with a collapse of the digital tunnel over the injured area. This incongruence between the repaired flexor tendons and the narrowed digital tube required a release of the retracted zone to restore an adequate volume. The only way reported is the "Venting" of a part or the total length of the pulley. This procedure even if it resolves the tendon gliding resistance, is still unacceptable. Indeed it destroys an important anatomical structure of the flexor tendon dynamic system. The flexor pulley Omega plasty "Omega" consists in releasing the lateral palmar attachment of the pulley enhancing its internal volume and increasing the flexor tendon gliding area. The digital tube is composed by the succession of five annular and three cruciform pulleys. The cruciform pulleys are thin and flexible. They retract during the digital flexion assuring the continuity of the digital tube, while the annular pulleys are thicker and fill a biomechanical function. There are two types of annular pulleys: the joint pulleys as A1, A3 and A5; they are attached to the palmar plates of the MP, PIP and DIP joints respectively. During the digital movement, they retract approximately 50% of their length. The osseous pulleys as A2 and A4 are fixed over the lateral and palmar borders of the first and the second phalanx respectively. It is on these pulleys that the Omega plasty is practised. The operative procedure is simple. It consists on a periosteal dissection over the one lateral border of the phalanx. The liberation is undergone palmarly releasing the lateral attachment of the pulley. It respects the anatomical continuity of the pulley and its mechanical properties. Indeed, the continuity of the pulley is fully respected with the periosteal flap of the digital tube floor maintaining sufficient attachment to the pulley to resist to the flexor tendon forces. The level of the flexor tendon injury and the digit position during the initial trauma will determine the level of tendon resistance and where the pulley plasty must be made. If the flexor zone II injury occurred with the digit in an extension position, the tendon conflict appears with the A2 pulley, while it arises with the A4 pulley if the digit was in flexed position. The Omega plasty creates the ideal conditions for an optimal flexor tendon movement recovery. It is a simple and a reproducible procedure. It doesn't distort the mechanical properties of the pulley and the digital tube. We used this pulley Omega plasty fifteen times in twelve patients. In 60% of the cases, the injury concerned the dominant hand, and in 67% of the cases, it was a work accident. In eight of our cases, the omega plasty was done in emergency at the same time of flexor tendon repair, while in the other seven cases, the pulley Omega plasty accompanied the late flexor tendon repair forgotten during the initial trauma management. In ten cases, the plasty concerned the A4 annular pulleys, while in the other five cases, it concerns the A2 annular pulleys. Four cases necessitate a secondary tenolysis three months after the tendon repair. Two patients moved out and cannot be included in our results. On the thirteen-remainder cases, nine retrieved a full digital flexion particularly those who underwent digital tenolysis, while the other four cases retrieved a satisfying digital function in spite of the partial DIP flexion. In our hand, the pulley Omega plasty "Omega" becomes almost a systematic procedure in conjunction with the flexor tendon repair. It offers the ideal conditions for a tendon healing and a physiological flexor tendons motion recovery.

Adult↗
PubMed2005

[The Omega "Omega" pulley plasty: a new technique for the surgical management of the De Quervain's disease].

The Omega "Omega" pulley plasty: a new technique for the surgical management of the De Quervain's disease. The De Quervain tenosynovitis is an inadequacy into the first extensor compartment between the osteo-fibrous tunnel and the tendons. This mechanical conflict generates a tenosynovitis of the extensor pollicis brevis and the abductor pollicis longus tendons. This is generally expressed by a tenderness on the radial side of the wrist over the radial styloid process. The medical management consists on corticoids infiltrations of the first extensor compartment, the avoidance of repetitive and stress movements of the first ray with the use of a rest splint. The surgical approach is considered with the recurrence of the painful symptoms. This well-known pathology is reputated to require a simple section of the pulley. Our post-operative complications have been reported in the literature of this classical surgical solution. These complications concern an incomplete release of the extensor pollicis brevis and the abductor pollicis longus tendons particularly when an extensor sub-compartment exists and was overlooked, an irritation of the collateral branches of the sensitive radial nerve or the occurrence of a nevroma after a nerve injury and the most serious complication is a palmar subluxation of the extensor tendons which can occur with the thumb extended and the wrist flexed. In rare cases, this subluxation can be really painful and requires a surgical management with secondary reconstruction of the pulley. This reconstruction necessitates distal pedicle flaps from the dorsal retinaculum or the brachioradialis tendon. To prevent these complications, Codega and Kapandji described techniques of reconstruction of the pulley after its release. More recently, Le Viet reported a procedure using the anterior flap of the pulley; fixed to the dermis it will work as a barrier and maintain the tendons sliding on the radial styloid groove. These techniques require to divide the pulley and to reconstruct it suturing the different flaps. It can generate adherences between the extensor tendons, the overlying skin and the collateral branches of the radial nerve. The authors present a new and original plasty procedure of the first extensor compartment pulley, the "Omega" Omega plasty. It consists to liberate the anterior attachment of the pulley over the anterior lip of the styloïd process respecting its continuity with the periosteum flap. This conservative procedure is very interesting; it permits enough expansion of the tunnel volume decompressing the extensor tendons as a treatment of the De Quervain disease and respecting the anatomy and the continuity of the osteo-fibrous tunnel. This technique is simple, reliable and respects the first ray extensor tendons gliding physiology and biodynamic. In spite of our short clinical experience with only ten cases, all the patients retrieve a normal function of the thumb with complete disappearance of the first ray tenderness and pain without any complications. These preliminary results are encouraging and push us to consider the "Omega" plasty as a first choice for the surgical treatment of the De Quervain tenosynovitis.

Humans↗
PubMed2005

[Introduction to the knowledge of subcutaneous sliding system in humans].

The mobility of our body structures is so intrinsic and natural to us that we tend to take it for granted. The very fact of being able to pinch your skin and lift it, then let it go and see it return to its initial shape and texture in just a few seconds may seem banal enough until you begin to think of all the elements involved. The same is true when you bend your fingers and think of the movement of the flexor tendon across the palm without external translation. For decades, scientists thought that the skin was simply an elastic structure with loose connective tissue and a more or less virtual space. However, in biomechanical terms, this explanation is very vague. These old concepts developed more than 50 years ago have evolved thanks to the impact of research at the microscopic level, and the global, mesospheric concept has been abandoned. And yet, surgical dissection in vivo demonstrates that there are only tissue connections, simply a histological continuum without any clear separation between skin and hypodermis, the vessels, the aponeurosis and the muscles. In fact, visible everywhere are structures, which ensure a gliding movement between the aponeurosis, the fat structures and the dermis. As they studied this system of gliding between the various organs, in particular at the level of the tendons, the authors noted the existence of a type of system composed of cables and veil-like structures that they term the Multimicrovacuolar Collagen Dynamic Absorption System (MCDAS). This system looks totally chaotic in organization and seems to function in a manner far removed from traditional mechanical structures. The functional unity of this sliding system is dependent upon a polyhedral three-dimensional crisscrossing in space of the microvacuoles, whose collagen envelope is type 1 or type 4 and whose content is made up of proteoglycoaminoglycans. The dynamic of this multimicrovacuolar system allows all of the subtle movements that occur within the body, thanks to its pre-stressed nature and the molecular fusion-scission-dilacerations that it is capable of. In this way, the system is mobile, can move quickly and interdependently, and is able to adapt is plasticity. This notion of microvacuoles is a fascinating one because it provides an explanation for the system's space-filling ability. The matter is composed of elements. However, although they seem to be arranged in a haphazard manner, this is not the case. In fact, they occupy space in an optimal manner. If we accept this notion of microvacuoles, then it becomes possible to explain certain pathologies occurring with age, such as edema, obesity, aging and inflammation. This sliding system is to be found everywhere in the body and would seem to be the basic network of tissue organization. For this reason, it should be thought of in global terms. Since it constitutes the inseparable link and occurs in all living structures and at many levels, could it be that it the basic architectural design of Life?

Adaptation, Physiological↗
PubMed2001

Macrophagic myofasciitis associated with inclusion body myositis: a report of three cases.

We describe three patients with macrophagic myofasciitis and inclusion body myositis. All patients fulfilled diagnostic criteria for inclusion body myositis and myopathologic criteria for macrophagic myofasciitis. In the three cases macrophagic myofasciitis complicated the evolution of a known and painless inclusion body myositis and was diagnosed in a repeated deltoid biopsy because of the appearance of myalgia during the course of inclusion body myositis in all cases. The unexpected appearance of myalgia during the course of painless inclusion body myositis must arouse the suspicion of an association of another inflammatory muscle disease, macrophagic myofasciitis.

Adult↗
PubMed2000

[True neurological thoracic outlet syndrome].

The thoracic outlet syndrome (TOS) encompasses various clinical entities affecting the neurovascular bundle crossing the thoracic outlet. Unfortunately, this term often proves to be confusing because many of these entities have little in common beyond their known or presumed lesion site. Neurogenic TOS (true TOS) is caused by compression of the lower trunk in the brachial plexus, the cervical ribs or fibrous band. This syndrome is extremely rare. We consider that this neurological form of TOS is a clearly defined neurological syndrome. We report 10 patients with true TOS. All were females. Stating the onset was difficult because symptoms were progressive and insidious. Pain was the most frequently reported symptom. Sensory deficit was slight or absent. All patients showed unilateral severe atrophy of the thenar muscles. Wasting and weakness developed later. A reduced amplitude of ulnar and median compound muscle action potential associated with a normal amplitude of median sensory nerve action and a reduced amplitude of ulnar sensory nerve action potential were indicative of a chronic axon loss in the lower trunk of the brachial plexus. In all cases, we performed medial antebrachial cutaneous sensory nerve action potential, a C8-T1 innervated nerve. The absence of the medial antebrachial cutaneous sensory nerve action potential in 9 patients and a reduction in amplitude of 50 p. 100 compared to the unaffected side in the other patient, indicated the diagnostic value of this easy and reproductible test. It confirmed a C8-T1 post-ganglionic radicular lesion or a lower brachial plexus neuropathy. Radiography showed a rudimentary bilateral cervical rib or an elongated C7 transverse process in all cases. Surgery was performed in the affected side in 7 patients and in each case the lower part of the brachial plexus was found to be stretched and angulated over a fibrous band, which was removed. Pain was relieved after 1 to 4 weeks. A minimal motor improvement was observed after one year. Electrophysiological results were unchanged.

Adult↗
PubMed1999

Spectrum of clinical and electrophysiologic features in HNPP patients with the 17p11.2 deletion.

OBJECTIVE: To study the clinical and electrophysiologic features of a large series of carriers of the 17p11.2 deletion. BACKGROUND: The 17p11.2 deletion is associated in most patients with recurrent acute nerve palsies, which is the typical presentation of hereditary neuropathy with liability to pressure palsies (HNPP). Nevertheless, a few other phenotypes have been reported. METHODS: On the basis of clinical and electrophysiologic data, the authors conducted a retrospective study of 99 individuals with the 17p11.2 deletion referred to their neurogenetic department between 1993 and 1997. RESULTS: In addition to the typical presentation of HNPP, they describe five other phenotypes in 15 patients: recurrent positional short-term sensory symptoms, progressive mononeuropathy, Charcot-Marie-Tooth disease-like polyneuropathy, chronic sensory polyneuropathy, and chronic inflammatory demyelinating polyneuropathy-like, recurrent subacute polyneuropathy; and 14 asymptomatic patients. In all the deletion carriers, regardless of their phenotype and by the second decade, the authors found a characteristic, multifocal electrophysiologic neuropathy consisting of a diffuse increase in distal motor latencies contrasting with normal or moderately reduced motor nerve conduction velocities, a diffuse reduction in sensory nerve action potential, and multiple focal slowing of nerve conduction at the usual sites of entrapment. The key diagnostic criterion is a bilateral slowing of sensory and motor nerve conduction at the carpal tunnel with at least one abnormal parameter for motor conduction in one peroneal nerve. CONCLUSION: The authors confirm the clinical phenotypic heterogeneity of the 17p11.2 deletion and suggest that electrophysiologic examination is a reliable tool for screening suspected HNPP patients in its various clinical presentations.

Adolescent↗
PubMed1999

[Distal Miyoshi muscular dystrophy in a Moroccan patient].

BACKGROUND: Muscular dystrophy usually involves a deficiency in the proximal muscles. We report a case of distal muscular dystrophy in a Moroccan patient. CASE REPORT: A 21-year-old Moroccan complained of progressive onset weakness of the lower limbs and frequent falls. The neurological examination demonstrated amyotrophy involving both legs and almost complete regression of the posterior muscle compartment. Clinical findings were confirmed by muscle scans. The electromyogram showed a progressive myogenic process. Creatine kinase was elevated. The severe dystrophic aspect was evidenced at muscle biopsy and led to the diagnosis of distal Miyoshi muscular dystrophy. DISCUSSION: Miyoshi muscular dystrophy, a distal myopathy transmitted by autosomal recessive inheritance, is usually observed in young adults who present characteristic amyotrophy of the posterior leg muscles. The proximal muscles of the lower and upper limbs may become involved during the disease course. Approximately one-third of the patients require wheel chair assistance after 10 years. Creatine kinase levels are constantly elevated. The differential diagnosis with other muscular dystrophies predominating in the distal muscles, particularly Steinert's myotonic dystrophy and inclusion body myositis, is discussed.

Adult↗
PubMed1997

Notch3 mutations in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a mendelian condition causing stroke and vascular dementia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited condition whose key features include recurrent subcortical ischemic events, migraine attacks and vascular dementia in association with diffuse white-matter abnormalities seen on neuroimaging. Pathologic examination shows multiple small deep cerebral infarcts, a leukoencephalopathy and a nonatherosclerotic nonamyloid angiopathy involving mainly the media of small cerebral arteries. To progress in understanding the pathophysiological mechanisms of this condition, we undertook the identification of the mutated gene. We mapped the CADASIL gene on chromosome 19p13.1. More than 120 families have been referred to our lab. Genetic linkage analysis of 33 of these families allowed us to reduce the size of the genetic interval to less than 1 cM and to demonstrate the genetic homogeneity of this condition. In the absence of any candidate gene, we undertook positional cloning of this gene. We identified, within the CADASIL critical region, the human Notch3 gene, whose sequence analysis revealed deleterious mutations in CADASIL families co-segregating with the affected phenotype. These data establish that this gene causes CADASIL. Identification of the CADASIL gene will provide a valuable diagnostic tool for clinicians and could be used to estimate the prevalence of this underdiagnosed condition. It should help in the understanding of pathophysiological mechanisms of CADASIL and vascular dementia.

Adult↗
PubMed1997

Loss of the presynaptic vesicle protein synaptophysin in hippocampus correlates with cognitive decline in Alzheimer disease.

We tested the hypothesis that synaptic defects in the hippocampus of individuals with Alzheimer disease (AD) correlate with the severity of cognitive impairment. Three postmortem groups were studied: controls with normal and stable cognition; cognitively intact subjects with senile plaque densities diagnostic for possible AD (p-AD) and neurofibrillary changes characteristic of early AD (Braak stage III); and individuals with definite AD and neurofibrillary changes typical of incipient to severe AD (Braak stage III, V, or VI). Synaptophysin (a presynaptic vesicle protein) levels were quantified by immunoblotting of synaptic membrane fractions isolated from hippocampus, entorhinal cortex, caudate nucleus, and occipital cortex. Average synaptophysin levels were reduced in hippocampus when comparing definite AD to controls (55%, p < 0.0001), p-AD to control (25%, p < 0.005), and definite AD to p-AD (30%, p < 0.05), but levels in entorhinal cortex, occipital cortex, and caudate nucleus were either unchanged or less significantly altered than in hippocampus. By univariate analysis, hippocampal synaptophysin levels correlated with neuropsychological measurements, including Mini-mental state examination scores (r = 0.83, p < 0.0001) and Blessed scores (r = 0.74, P < 0.001), and with senile plaque densities (r = 0.89, p < 0.0001). We conclude that synaptic abnormalities in the hippocampus correlate with the severity of neuropathology and memory deficit in individuals with AD, and that this defect may predate neuropsychological evidence for cognitive impairment early in AD.

Aged↗
PubMed1996

Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia.

Stroke is the third leading cause of death, and vascular dementia the second cause of dementia after Alzheimer's disease. CADASIL (for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) causes a type of stroke and dementia whose key features include recurrent subcortical ischaemic events and vascular dementia and which is associated with diffuse white-matter abnormalities on neuroimaging. Pathological examination reveals multiple small, deep cerebral infarcts, a leukoencephalopathy, and a non-atherosclerotic, non-amyloid angiopathy involving mainly the small cerebral arteries. Severe alterations of vascular smooth-muscle cells are evident on ultrastructural analysis. We have previously mapped the mutant gene to chromosome 19. Here we report the characterization of the human Notch3 gene which we mapped to the CADASIL critical region. We have identified mutations in CADASIL patients that cause serious disruption of this gene, indicating that Notch3 could be the defective protein in CADASIL patients.

Adult↗
PubMed1996

[Longstanding flexor tendon lesions treated by two-stage tendon graft].

46 fingers in 42 patients undergoing 2-stage flexor tendon grafting for traumatic injury in zone 2 were evaluated with an average follow up of 13 months (range 6 to 120 months). 24 anastomoses between FDS and FDP were performed according to the Paneva Holevitch procedure. In all other cases, palmaris longus or plantaris were used as tendon grafts during the second stage. Proximal fixation was always performed in the palm. 3 or more pulleys were reconstructed in all cases. In 21 cases, pulley reconstruction required the use of excised tendon remnants or retina-culum dorsalis. Distal fixation was performed to the distal phalanx in 42 cases and to the second phalanx in 4 cases, during the second stage. Overall, 85% patients obtained a good or fair result in terms of TAM (total active motion) with < >. 7 cases obtained a poor result. 12 fingers required complementary surgery: --2 cases with poor active flexion had been treated by shortened suture. --3 ruptures of tendon graft required P2 fixation and DIP arthrodesis in distal rupture (2 cases), and anastomosis with next flexor tendon in proximal rupture (1 case). --7 cases of PIP stiffness were treated by PIP arthrolysis. DIP arthrodesis was associated in 2 cases.

Adolescent↗
PubMed1996

[Hypothermia and the nervous system. Review of the literature apropos of 4 cases].

Thermoregulation involves a long term adaptation system with hormonal processes and an immediate regulation system by extrapyramidal tracts, sympathetic part of autonomic nervous system and cortical integration of body temperature changes. Both system are under control of a hypothalamic center. Prolonged accidental exposure to intense cold and myxoedematous coma are the best known etiologies of hypothermia. However milder and often misdiagnosed hypothermia can occur at home in patients without endocrinologic disease. In these cases, hypothermia is due to dysfunction of immediate thermregulation under neuronal control, especially somatomotor and autonomic system. We report four cases of hypothermia of this kind. Two patients had an inhibition of peripherical mechanisms of protecting against cold (cutaneous vasoconstriction, shivering) and had dampened perception of cold: one was 73, had diabetes mellitus and took different drugs, the other one suffered from systemic lupus with myelopathy. The two other patients probably had a disorder of the thermoregulation hypothalamic center: one had Wernicke's encephalopathy and the other multiple sclerosis. From these cases and a review of the literature, we describe the different etiologies of hypothermia and their pathophysiology.

Adult↗