Discussion in 'JF Doctor' started by Isimilo, Jun 25, 2010.
naomba kujua tiba ya kiharus
kiharusi???to The best of my KNOWLADGE harusi hushangiliwa kwa kupungiwa mikono,.na wengine hunyanyua miguu...wagonjwa ni wengi,.....
kiharusi ndio stroke?
inakaribiana na hiyo PRETA,.ingawa vyanzo vya dalili hiyo ni vingi,..neural paralysis,.epilepsy.,korea witingngton.,.Myasthenia gravis.,..epilepsy n.k.bila kujua asili ya ugonjwa itabidi ;./du
Kiharusi ni ugonjwa wa kupooza upande mmoja Au kwa kiingereza unaitwa (
Facial Nerve Paralysis, Dynamic Reconstruction
Author: Alan Bienstock, MD, Consulting Staff, Division of Plastic and Reconstructive Surgery, Department of Surgery, Lennox Hill Hospital, St Luke's/Roosevelt Hospital
Coauthor(s): John YS Kim, MD, Assistant Professor, Department of Surgery, Division of Plastic Surgery, Northwestern Medical Faculty Foundation; Consulting Staff, Northwestern Plastic Surgery; Mary C Snyder, MD, Associate Professor, Division of Plastic Surgery, University of Nebraska Medical Center; Perry J Johnson, MD, Assistant Professor, Department of Plastic and Reconstructive Surgery, University of Nebraska Medical Center
Contributor Information and Disclosures
Facial nerve denervation and paralysis imposes significant psychological and functional impairment. Facial paralysis can inhibit and mar facial expression, communication, symmetrical smile, eye protection, and oral competence. Myriad modalities and stratagems exist for each patient; the physician must accurately evaluate and examine the patient and determine the etiology, duration, and the scale of the paralysis. Understanding facial nerve anatomy with precise assessment of the patient's paralysis and health status dictates the potential for recovery and the most appropriate reconstructive scheme.
The goals of the reconstruction in facial paralysis include the following:
Facial symmetry at rest
Voluntary, coordinated, spontaneous facial movements
Oral competence and eyelid closure with corneal protection
Absence or limitation of synkinesis and mass movement
Dynamic and static procedures are employed for facial reanimation; however, dynamic strategies tend to be more successful and fruitful and should be offered to each patient considering reconstruction, unless health risk contraindications exist. The most common approaches for reconstruction are direct facial nerve repair with or without grafting, nerve transfer, cross-facial nerve grafting, and muscle transfer (either regional muscle or free-muscle neurotized transfer). Anatomy of the Facial Nerve
The precentral gyrus emits the voluntary motor portion of the facial nerve, where most of these nerve fibers cross in the pontine region to approach the facial nerve nucleus in the contralateral pons. At the cerebellopontine angle (CPA), the facial nerve is near the nervus intermedius and the eighth cranial nerve.
Intratemporal facial nerve
The first branch of the facial nerve is the greater petrosal nerve, which departs from the geniculate ganglion and is responsible for parasympathetic secretion of the nose, mouth, and lacrimal gland. The nerve to the stapedius is the next branch and arises from the proximal mastoid segment. The chorda tympani nerve emerges proximal to the stylomastoid foramen and carries parasympathetic secretory fibers to the submandibular and sublingual glands as well taste fibers to the anterior two thirds of the tongue.
Extratemporal facial nerve
The extratemporal branching of the facial nerve has myriad patterns and variations. Dingman and Grabb present the largest series of the surgical anatomy of the marginal mandibular branch,1 while Pitanguy identifies the course of the temporal branch.2
The facial nerve innervates a total of 23 paired muscles and the orbicular oris, but only 18 of these muscles, working in a delicate balance, produce facial animation and expression. No current reconstructive stratagem can reproduce every facial expression and movement.
Evaluation of a patient with facial paralysis commences with a thorough and detailed history and physical examination. Etiology is the most important factor in determining the timing and choice of reconstructive technique. Reconstructive efforts should not commence prior to establishing the etiology of the paralysis.
A thorough history includes onset, initial degree of paralysis, duration, and associated symptoms. These details often can help identify the etiology. Facial nerve injuries from Bell palsy, trauma, and malignant neoplasm need to be identified. The reconstructive efforts and interventions need to be tailored appropriately based on the etiology of the disorder.
For example, a slowly progressive paralysis suggests malignancy, while a sudden onset of complete paralysis suggests Bell palsy. The workup, treatment, and prognosis of these 2 disorders differ vastly from one another. If a tumor is suspected, proper evaluation of the patient is of the utmost importance to appropriately treat the malignancy and choose the best reconstructive option. If paralysis is caused by a malignancy or is a result of resection for a malignancy, the risk of recurrence and prognosis may influence the choice of reconstruction. Malignancy of the posterior fossa, temporal bone, skull base, or parotid region can present with facial paralysis.
Bell palsy is an idiopathic form of facial paralysis and is a diagnosis of exclusion. Trauma is the second most common cause of facial paralysis. Eighty percent of patients with facial paralysis suffer from Bell palsy. Eighty-five percent of these patients begin to recover nerve function spontaneously within 3 weeks of onset; the other 15% do not have any movement for 3-6 months. If the patient has Bell palsy, the potential for complete recovery is excellent, especially in incomplete paralysis. Peitersen found 94% of patients with partial paralysis completely recovered facial nerve function in 1 year without medical or surgical intervention; of those with complete paralysis, 71% completely recovered.3 Therefore, irreversible techniques to reanimate the face may not be the best choice in these patients.
The etiology of the denervation also dictates the timing of surgical treatment, if any is to be done. In a patient with a paralyzed face secondary to traumatic surgical disruption, the surgeon should initiate reconstruction as soon as possible, generally within the first month. On the other hand, a patient with an intact nerve can be monitored for recovery for up to 12 months. The duration of the facial paralysis is essential. The reconstructive options for acute paralysis, paralysis for less than 18-24 months, and paralysis for greater than 18-24 months differ significantly.
In addition, the surgical team must investigate previous surgical procedures for reanimation, since these may limit reconstructive options. The patient's overall health, psychological stability, and life expectancy are significant considerations. Patients with significant health risks and medical problems are not appropriate candidates for invasive reconstructive operations, the results of which do not manifest for 2-3 years postoperatively. The patient and the surgeon should thoroughly discuss the patient's expectations. As part of patient education, surgeons need to establish realistic expectations and determine whether the patient is willing to expend the time and financial resources required for a successful result.
The surgeon must perform a comprehensive physical examination of the patient with facial paralysis, scrutinizing the face at rest and during voluntary and reflex emotional movement. The physician must determine the involvement of unilateral or bilateral facial nerves, facial asymmetries, and synkinesis. The degree of brow ptosis, ectropion, lid laxity, and oral competence must also be noted. The surgical team cannot neglect other cranial nerve or neurologic deficits and soft tissue defects in conjunction with the paralysis.
Audiometric testing, including acoustic reflexes and tympanometry, may be useful in identifying the etiology of facial palsy secondary to retrocochlear pathology or mass lesions of the middle ear.
High-resolution CT and MRI scans are essential in the evaluation of a patient with traumatic facial nerve palsy to delineate features of the temporal bone, which may impact the facial nerve. Scans are also used to evaluate patients with possible parotid, skull base, temporal bone, intracranial, or extratemporal tumors.
Electrodiagnostic tests of nerve function
Electrodiagnostic tests of facial nerve function include nerve excitability tests (NET), electroneuronography (ENog), and electromyography (EMG). Nerve excitability testing involves percutaneous stimulation of the facial nerve until muscle contraction is observed. The minimal NET determines the threshold stimulation required for muscle contraction compared to the unaffected side. Maximum stimulation test (MST) is a modification of the NET but is a supramaximal stimulus compared to the unaffected side, and the stimulus is increased until the patient encounters discomfort. The subjective nature of the measurements and lack of recorded data limit both methods, and they do not reflect denervation at the moment it is occurring.
Electroneurography (ENog) is an objective measure of facial nerve function that measures the amplitude of evoked compound muscle action potentials (CMAP) with electrodes over the skin of the nasolabial fold. The compound action potential is compared between the 2 sides of the face, and the response of the affected side is expressed as a percentage of the response of the unaffected side. A percentage of nerve fiber degeneration is calculated. A 95% decrease in CMAP compared with the contralateral side signifies a 50% chance that the patient will have unsatisfactory recovery of facial nerve function. Surgery is indicated if a 90% decrease in CMAP is reached within the initial 2 weeks of the onset of paralysis. ENog is objective and is the most accurate reproducible test, but it is expensive and time-consuming.
EMG is a measure of volitional muscle response unlike the other modalities. Needle electrodes are used to monitor activity of the facial muscles. Normal muscle exhibits activity upon needle insertion, electrical silence at rest, and diphasic or triphasic action potentials during voluntary contraction. Fibrillation potentials are observed in the denervated muscle, and polyphasic potentials are observed in muscle undergoing reinnervation. Complete electrical silence is observed in denervated muscle with significant fibrosis. EMG is useful in evaluating patients with acute or traumatic nerve injury and in assessing the viability of the facial musculature when evaluating patients for reinnervation procedures. EMG does not show any signs until 3 weeks after paralysis and should not be utilized until 3 weeks after facial paralysis without any signs of recovery.
Objective measures of facial motion
Objective measures of facial motion include digital photography and video recording of the patient and rest and during motion. Dated visual documentation and preoperative and postoperative facial function is salient for preoperative planning and outcome assessment.
A recently developed method of objective measurement is the maximum static response assay of facial motion. This method quantifies facial motion preoperatively and serially during the postoperative period. Mark the patient's face and ask him or her to perform region-specific movements, including brow lift, eye closure, smiling, frowning, and whistling or puckering. The images of the face in repose and the maximum response movements are recorded and processed for computer display. The images are calibrated and normalized, and vectors of movement are determined and measured using a grid and an internal facial coordinate system. Even slight improvements in facial movement can be detected over the long recovery periods that often accompany facial reanimation procedures.
Patients desire a countenance and visage with a normal or almost normal balance when the person's face is at rest. Objectives of treatment are corneal protection, establishing a normal resting tone, and, most importantly, restoring a symmetrical dynamic smile.
Little information is available on the denervation of human facial muscles. Denervated muscles cannot be voluntarily stimulated and has no response to electrical stimulation. A longer period of denervation translates into a lesser degree of recovery after reinnervation. There is a decrease in efficiency of muscle reinnervation after 12-18 months of paralysis/denervation. Muscles that are reinnervated may not undergo full recovery nor respond to regenerated nerves.
Repair of the facial nerve is the most effective procedure to restore the function of the face. Repair is indicated in patients who have experienced acute disruption or transection of the nerve from an accident, trauma, resection during extirpation, or inadvertent division during surgery.
Principles of Nerve Repair
Early identification and repair of nerve injuries
The most critical factor in achieving good postoperative facial function is early identification and repair of nerve disruption. Several investigators have demonstrated that earlier repair of the facial nerve produces superior results. Some authors report function in patients who were grafted 18-36 months after injury, but superior results are found with repairs performed within 1 year. May advocates repair within 30 days. This recommendation is based on clinical results and neurobiologic investigations that reveal that the regenerative process begins almost immediately following injury.
Following axotomy, the nerve cell body immediately undergoes changes in morphology and protein synthesis to support axonal replacement. The proximal portion of the interrupted axon transforms into a growth cone, and, within a few days, axon sprouts push out, seeking the distal motor endplate. Neuron metabolic activity peaks approximately 21 days after injury. The distal portion of the interrupted axon undergoes Wallerian degeneration, and, within 2 weeks, collagen and scar tissue begin to replace axons and myelin in the distal nerve stump.
Traumatic nerve injuries must be repaired expediently. In the instance of a grossly contaminated wound (eg, shotgun injury), the nerve ends can be tagged and repaired at a later date. A nerve accidentally transected during surgery (eg, facelift) should be attacked with an end-to-end anastomosis. If the facial nerve is resected because of tumor involvement, frozen sections of both ends can be sent for histopathologic examination to exclude microscopic invasion before attempting repair. When margins are clear, either end-to-end anastomosis or graft repair can be performed immediately.
Evaluation of nerve condition
The condition of the nerve at the time of injury dictates whether nerve repair is indicated and whether it will presage functional repair. The condition of the nerve depends on the type of injury or trauma. A patient with preoperative facial palsy secondary to tumor involvement of the facial nerve is unlikely to experience a good result following resection and repair. The amount of functioning nerve fibers at the time of surgery does not increase after repair; do not expect improved postoperative facial function over preoperative status.
A sharp facial nerve laceration from glass or a knife should be suitable for end-to-end anastomosis. Gunshot wounds, however, either crush or avulse the nerve, which propagates further nerve degeneration/denervation. These injuries should not be repaired in the immediate setting until the extent of the nerve damage has declared itself. In a delayed intervention, scar tissue and neuromas must be removed, and unhealthy nerve ends must be excised. Identifying healthy nerve stumps may necessitate histologic or microscopic confirmation.
Matching of endoneurial surfaces
Matching of the endoneurial surfaces is essential in promoting neural regeneration and is more important than a match of the total nerve diameter. The endoneurium is examined more easily by removing the overlying perineurium at the ends of the nerve. Occasionally, a significant mismatch between proximal and distal nerve ends requires a double cable graft (eg, when grafting from the main facial nerve trunk to segmental branches).
Epineural versus perineural suturing
Various neurorrhaphy techniques and adjunctive measures have been investigated in attempts to improve neural regeneration, including epineural versus perineural sutures, tissue adhesives, laser neurorrhaphy, tubulization, and trophic factors. However, the most efficacious method of re-approximation remains unproven, and no specific adjunctive measure has been found to be beneficial. A minimal number (usually 2 or 4) of epineural or perineural sutures, using a fine monofilament suture under microscopic vision, or loupe magnification, remains the time-tested criterion standard for nerve repair.
Tension-free anastomosis and nerve grafts
Primary neuropathy can be achieved if the proximal and distal facial nerve ends can be approximated without tension. If tensionless nerve repair is not feasible, then a nerve graft (usually the sural nerve) will be interposed in between the proximal trunk and distal branches. Any tension on the ends after repair results in the formation of scar tissue and poor neural regeneration. Mobilization of the nerve may add up to 2 cm of relative length but also may result in devascularization and further neural injury. Any defect greater than 2 cm should be tackled with a nerve graft. The surgeon must design the nerve graft of adequate length without any tension and with a small amount of slack when bridging the defect.
Cable grafts function as conduits in which sprouting axons from the proximal nerve stump travel to the motor endplates. The graft provides cellular and humoral promoters for neural growth, such as Schwann cells, extracellular matrix, and neurotrophic growth factor.
Success of a nerve graft depends on the following factors:
The number of axons remaining in the nerve
The potential for regeneration of axons
The status of the facial muscles (ie, the more axons that are available, the greater chance of recovery and a satisfactory result)
Donor Nerves for Facial Nerve Grafting
The great auricular nerve and sural nerve are the most commonly selected nerves for facial nerve grafting. Disadvantages include a sensory deficit of the earlobe when using the great auricular nerve or of the lateral foot when using the sural nerve. The great auricular nerve is harvested easily; since it is located near the surgical field in which the nerve repair is taking place, it tends to be a good match in size, and its extensive arborization allows the anastomosis of the proximal facial nerve stump to several segmental branches. However, only 7-10 cm of the great auricular nerve can be harvested safely, which limits its use in extensive repairs. The sural nerve is larger, with a greater axonal volume, and up to 35 cm is harvested easily from the posterior lower leg. It is especially useful in cross-facial grafting.
The principles and technique of graft anastomosis are identical to those of primary repair. The patient should not expect return of facial function following nerve grafting for 4-6 months, as regenerating axons travel a distance of approximately 1 mm/d. Improvement in function can be expected for up to 2 years. In general, results after nerve grafting are not as good as those observed with primary repair. Spector et al found incomplete reinnervation of facial divisions, decreased voluntary contractions, and more severe synkinesis when comparing cable grafts to direct end-to-end anastomoses.4 However, 92-95% of patients who undergo facial nerve grafting experience some return of facial function, and 72-79% have good functional results.
Location of Injury
Intracranial nerve injury most commonly occurs during resection of an acoustic neuroma or other tumor of the cerebellopontine angle (CPA). Prior to the advent of the operating microscope in 1961, rates of facial palsy following acoustic neuroma removal approached 95%. House, by implementing the use of the operating microscope, reported a 72% rate of normal facial function in patients who underwent tumor resection from 1961-1968.5 More recently, a 97.7% rate of facial nerve preservation following CPA tumor surgery was reported.
In the event of nerve injury in the CPA, immediate repair with direct anastomosis or graft is advocated. Rerouting the tympanic and mastoid segments of the nerve may add enough length for end-to-end anastomosis, but a graft is often required. Interposition grafts can be placed from the intracranial nerve segment to the temporal segment or from the intracranial nerve segment to the extracranial segment, thus bypassing the temporal bone. These repairs are technically difficult. The proximal nerve end, as it enters the brain stem, usually is short and has no epineurial covering. The brain stem is pulsatile, and cerebral spinal fluid constantly flows through this area. However, despite the difficult nature of intracranial repair of the facial nerve, it is a highly reliable technique to restore facial function. Arriaga and Brackmann report that 87.5% of patients who undergo this type of repair developed some degree of facial function, with 57% achieving grade IV or better.6
Intratemporal facial nerve injury is observed in patients who experienced external head trauma or iatrogenic injury during otologic procedures. Temporal bone fracture is the most common mechanism of facial nerve injury from external trauma. Most temporal bone fractures result from motor vehicle accidents, and 7-10% of these fractures result in facial nerve dysfunction. In temporal bone trauma, facial nerve injury most often occurs in the perigeniculate and labyrinthine areas with axonal degeneration extending a variable distance, possibly involving the entire intratemporal length.
Management of facial nerve injury following temporal bone trauma remains controversial. However, a review of the literature concludes that patients with complete paralysis at the time of injury have a poorer prognosis than those with incomplete or delayed paralysis. Chang and Cass propose a reasonable algorithm for management of intratemporal facial nerve injury, in which patients with delayed onset or incomplete paralysis are observed. If the paralysis progresses to complete paralysis, perform serial ENog.7 In addition, monitor patients with immediate complete paralysis with serial ENog. If ENog shows greater than 95% degeneration in the first 14 days after injury, offer the patient facial nerve exploration and decompression. Explore the entire length of the nerve from the meatal foramen to the stylomastoid foramen. Perform nerve repair via primary anastomosis or graft only if total or near-total transection is certain.
Intratemporal nerve injury occurs in 0.6-3.6% of otologic procedures. A review by Green et al revealed mastoidectomy, with or without tympanoplasty, as the most common otologic procedure resulting in facial nerve injury.8 Green et al also reported injury of the facial nerve during tympanoplasty alone and during removal of exostoses.8 Patients with previous surgery, infection, tumor, or congenital anomalies of the ear are at a higher risk for inadvertent nerve injury. If the injury is recognized immediately, repair it during the primary procedure. Explore a postoperatively recognized facial paralysis that does not recover over several hours. Monitor a delayed-onset paralysis with serial ENog and explore if more than 90% degeneration occurs within the first week. Strongly consider nerve repair if more than 50% of the nerve is transected.
Extratemporal injury to the nerve may occur during surgery of the parotid or submandibular gland, temporomandibular joint procedures, or facelift procedures, or from traumatic lacerations of the face. Paralysis of the facial nerve following uncomplicated parotid procedures is reported at a 20% rate of temporary palsy, with a 10% rate of permanent paresis of temporal or mandibular branches. Children are at higher risk for facial nerve injury during parotid surgery, as are patients who undergo total parotidectomy. Surgery of the parotid gland often is performed for benign or malignant tumors that may involve the facial nerve. If the nerve is resected because of a tumor, histopathologic confirmation of clear margins is required prior to repair by direct anastomosis or graft.
Inadvertent transection recognized during facelift or parotid surgery warrants immediate primary repair. Postoperative paralysis with known facial nerve integrity usually recovers within 6 months of the procedure. Traumatic transections, iatrogenic injuries, and division of segmental branches proximal to the lateral canthus should be explored and repaired. Facial nerve injury following submandibular gland surgery, which usually involves the marginal mandibular branch of the nerve, is not uncommon. Sacrifice of this branch may be unavoidable because of involvement by the disease process, most commonly chronic infection or tumor. Temporomandibular joint procedures may injure the temporal branch or, less commonly, the main trunk of the facial nerve. Facial nerve injury during rhytidectomy is rare, usually temporary, and most often involves the segmental branches.
The surgeon is obliged to explore traumatic or iatrogenic transections that involve the main trunk of the facial nerve and repair them as soon as they are recognized. The surgeon should explore and repair segmental branches proximal to the lateral canthus and nasolabial fold. Medial to the lateral canthus, extensive interconnections between the zygomatic and buccal branches provide neurotization of denervated muscle and satisfactory functional recovery. Nonetheless, the surgeon should also explore and repair medial temporal and marginal branch injuries, if possible. Nerve Substitution and Grafting
Nerve substitution via grafting or nerve transfer should be achieved in patients with facial paralysis who lack the proximal nerve segment but have an intact distal neuromuscular pathway, including an intact distal segment of nerve and facial musculature suitable for reinnervation. A donor nerve, transferred and anastomosed to the distal facial nerve stump, innervates the facial muscles in place of the injured proximal facial nerve.
The spinal accessory, phrenic, and trigeminal nerves have been used in nerve transfer procedures. However, sacrificing these nerves involves significant morbidities. Therefore, the hypoglossal nerve transfer/graft and cross-facial grafting have remained the mainstays in treatment.
Selection of Patients
Eighteen months after the original nerve injury, the facial muscles atrophy and do not regain any modicum of function. When the interval of facial nerve dysfunction is less than 18 months, primary repair, nerve grafting, or nerve transfers can be explored. Denervated facial musculature undergoes atrophy immediately after nerve injury and takes several years to complete. If the status of the facial musculature is in question, the team should perform electromyography (EMG), muscle biopsy, or both prior to the reinnervation procedure.
Proximal facial nerve segment
Several factors must be considered when selecting patients for nerve substitution. The availability of the distal neuromuscular unit is the most essential requirement for this technique. Unavailability of the proximal facial nerve segment most commonly occurs following cerebellopontine angle (CPA) surgery, in which the nerve is resected at the brain stem or, occasionally, following radical or ablative procedures for tumors of the parotid gland, temporal bone, or skull base.
Intact distal neuromuscular unit
The surgeon must evaluate the distal neuromuscular unit. Denervated facial musculature undergoes atrophy and eventual fibrosis in a process that begins immediately after nerve injury and takes several years to complete. As stated above, if the status of the facial musculature is in question, perform EMG and muscle biopsy prior to the reinnervation procedure. The distal nerve stump also undergoes degeneration as previously described, and severe neurofibrosis may limit axonal regrowth.
Suitable donor nerve and loss of donor nerve function
Nerve transfer always results in either total or partial loss of function in the donor nerve, depending on the technique used. Hypoglossal substitution results in paralysis or weakening of the ipsilateral tongue muscles, which may result in significant problems with speech, mastication, and swallowing.
Direct hypoglossal-to-facial graft
Korte performed the first hypoglossal-facial nerve anastomosis in 1901.9 May reports improvement of tone and symmetry in more than 90% of patients who undergo this procedure. Initial results usually are observed within 4-6 months, indicating the amount of time necessary for axons to travel to the distal motor endplate. Voluntary movement develops and continues to improve for up to 2-3 years.
Spontaneous, symmetric movement is unlikely following this type of procedure. Patients must undergo biofeedback and motor sensory re-education to learn voluntary control of movement, decrease synkinesis, and limit facial grimacing that can occur with mastication.
The team evaluates function of the facial nerve following hypoglossal-facial anastomosis by the degrees of tone, symmetry, movement, and synkinesis exhibited rather than by the traditional House-Brackmann scale. A review of several large series of patients found that 42-65% experienced good-to-excellent results, which were described as the presence of tone and symmetry, with fair-to-good movement and moderate-to-mild synkinesis.
Complications following hypoglossal-to-facial anastomosis include variable degrees of hemitongue atrophy and functional disability, including difficulty with chewing, swallowing, and speaking. In general, these impairments improve over time, and many patients report fewer problems chewing postoperatively than preoperatively. This likely is due to improvement of buccal tone.
Partial hypoglossal-to-facial jump graft
A partial hypoglossal-to-facial nerve transfer using a jump graft can reanimate the facial muscles while curbing the complications of complete hypoglossal sacrifice. In this technique, a cable graft is anastomosed in a notch in the hypoglossal nerve and attached to the intact facial nerve stump using microsurgical principles.
May analyzed results and complications between cranial nerve XII-VII direct-transfer and XII-VII jump-graft techniques and found that only 8% of patients undergoing jump grafting experienced permanent tongue deficit, compared to 100% of nerve transfer patients. Good facial movement and expression was noted in 41% of jump graft patients, and they experienced less synkinesis than the nerve transfer patients.10 Facial motor function generally is not as strong following a jump graft, and recovery of facial function was found to take longer in jump grafts.
Cross-facial nerve graft
Smith and Scaramella first reported cross-facial nerve grafting in 1971. This technique provides the potential for symmetry and involuntary mimetic function. Disadvantages include weakening of the contralateral facial nerve and inadequate power to innervate the ipsilateral musculature. Cross-face nerve grafting is indicated if the proximal ipsilateral facial nerve is not available but the distal stumps are available. Outcome of cross-nerve grafting depends on timing and technique and can provide the best facial reanimation scheme if performed on the right patient.
The surgeon must select appropriate segmental branches of the contralateral facial nerve as donors, with the sural nerve serving as a cable graft. Many techniques have been described, such as a single segmental-to main trunk anastomosis and multiple anastomoses from segmental branches to segmental branches. The grafts are tunneled above the supraorbital ridge for the orbicularis oculi, the upper lip for the zygomatic and buccal branches, and below the lower lip for the marginal mandibular branch.
Facial muscle movement will not emerge until 9-12 months after the procedure (ie, the allotted time for axonal growth to cross the graft). Cross-facial nerve grafting remains polemic, and many investigators relegate it as an adjunctive procedure in combination with other reanimation strategies.
When facial nerve dysfunction has exceeded 18 months, dynamic slings and free muscle transfers can be executed to restore facial and oral motor function. Severe neurofibrosis and myofibrosis in the distal neuromuscular unit preclude successful reinnervation. Patients with congenital facial paralyses cannot be reinnervated, since the neuromuscular units never developed. Regional muscle transposition and free-muscle transfer are the 2 modalities to reanimate the face in this subset of patients.
Regional muscle transfer can reanimate the lower third of the paralyzed face. This new neuromuscular unit is composed of the transferred muscle (to its new origin) with its original nerve and vascular supply.
The temporalis muscle may improve the symmetry of the commissure of the mouth and reestablish a voluntary smile. The vector of the temporalis muscle resembles that of the zygomaticus major and, thus, results in a lateral smile.
Temporalis muscle transposition can also reanimate the eyelids. Reanimation of the eye with the temporalis transfer can produce eyelid distortion. To avoid a contour defect, do not use the muscle anterior to the hairline. Transposition will not produce spontaneous mimetic function. Each movement necessitates a specific volitional action, in which the patient must consciously contract the transposed muscle in conjunction with the smiling. Reanimation of the eye with the temporalis muscle can cause eyelid distortion.
The muscle is harvested through a vertical incision in front of the ear that extends to the scalp. The middle section of the muscle and fascia is elevated and detached superiorly from the skull while preserving the inferior attachments. Two tongues are creating by bisecting the muscle, and the muscle is tunneled through a subcutaneous pocket from the zygomatic arch to the vermillion border. The ends of the temporalis are secured to the orbicularis and the corner of the mouth. The ends should be secured with enough tension to create some level of overcorrection. The patient initiates a smile by consciously tensing the temporalis muscle. Patients will require therapy to master this technique.
In his study, May reports improvement in 95% of patients with temporalis transfer for lower face reanimation and good-to-excellent results in 78% of patients. The complication rate was 18%; the most common complications were infection and implant-related complications. Other potential complications include failure of attachment, pulling away of the temporalis muscle from the commissure, and overcorrection of the upper lip. The transfer may also generate excess muscle bulk and a facial deformity, particularly over the zygoma.
The masseter muscle is another muscle used for reanimation of the commissure of the mouth, either alone or in conjunction with the temporalis. Unlike the temporalis, the vector of smile of the masseter muscle is in the buccinator-risorius direction, which produces a less natural smile. This muscle is elevated by detaching the anterior portion from its mandibular insertion. It is similarly bisected and secured to the modiolus. The muscle is quite bulky and can create facial irregularity or surface deformity, such as a bulge at the commissure. Postoperatively, patients must train the masseter with aggressive physical therapy to learn how to use the transposed masseter to produce a smile.
The smile is one of the most important facial expressions, and facial paralysis can debilitate an individual. Conley developed the modern method of transposing the tendon of the digastric muscle to the orbicularis of the lower lip. The blood supply and nerve to the anterior belly remains intact, and dynamic depression of the lower lip border is achieved. Of 36 patients treated in this manner by Conley, 33 were reported to have satisfactory results. This method is ideal for isolated palsy of the marginal mandibular nerve only, since it can create oral incompetence in patients with more extensive palsy of the lower face.
Depressor muscle function is important to dentured smile as well as to expressions of sadness, anger, and sorrow. The lower lip is animated by interactions of the orbicularis ori, depressor labii inferioris, depressor anguli oris, mentalis, and platysma. Terzis describes a technique to improve this type of smile by transfer either of the anterior belly of the digastric tenor or of the platysma.11 Other authors argue that this symmetrical smile could be achieved with less invasive approaches, including BOTOX® injections or myectomy of the depressor labii inferioris.
Regional muscle transposition is limited by anatomic constraints of size and vectors and often produces results slightly better than static strategies. Regional muscle procedures are appropriate in patients who are in poor health or who will not survive beyond the 12-24 month period of neurotization of a free muscle transfer. Such procedures provide immediate reanimation and are technically less demanding than cross-facial nerve grafting with free muscle transfer.
Principles of Free-Muscle Transfer
Cross-facial nerve grafting with microneurovascular muscle transfer is the best strategy for facial reanimation when a patient has long-established facial paralysis (>24 mo). Other approaches leave residual asymmetry, an unnatural appearance, and unwanted facial movements while eating. The advent of microsurgical technique and free-muscle transfer ignited a new epoch for facial reconstruction in patients with chronic facial palsy. Free-muscle transfer supplies a new neuromuscular unit to the face via a free-muscle flap and a grafted donor cranial nerve, usually a cross-facial nerve graft. This modality establishes more precise vectors in addition to spontaneous mimetic facial expression. Most commonly, the surgeon executes a 2-stage technique of cross-facial nerve graft followed by a delayed free-muscle transfer. The rationale for the delay is to prevent atrophy of the muscle graft while waiting for axons to travel the length of the nerve graft.
Cross-facial nerve graft
Occasionally, the proximal segment of the ipsilateral facial nerve is available for grafting to innervate a free-muscle transfer. This situation most commonly occurs in the event of a failed interposition nerve graft, resulting in facial musculature that no longer can be reinnervated.
The contralateral facial nerve is chosen as the donor nerve, and a redundant zygomaticus branch is selected for grafting. The hypoglossal nerve also can act as a donor, either by a direct or jump graft alone or in conjunction with a cross-facial graft. The sural nerve is anastomosed to the contralateral facial nerve or substituted cranial nerve and tunneled subcutaneously from the donor nerve to the planned site of free-muscle transfer and the distal segment of the graft is tagged. The ideal time for the muscle transfer occurs when a Tinel sign is detected in the distal nerve end, indicating completion of axon growth.
Muscles suitable for transfer
Free-muscle transfer is usually performed 9-12 months after nerve graft. A plethora of muscles have been assiduously investigated for free transfer to the paralyzed face, including the gracilis, serratus, pectoralis minor, latissimus dorsi, platysma, rectus abdominis, rectus femoris, and extensor digitorum brevis.
The original report by Harii in 1976 of free-muscle transfer for facial paralysis described use of the gracilis muscle.12 It remains the muscle of choice because of its relative ease of dissection, adequate neurovascular pedicle, and muscle fiber length, which corresponds to the action of the zygomaticus major muscle. The vascular pedicle is derived from the medial femoral circumflex artery and provides up to 8 cm of length. Innervation of the gracilis is provided by the anterior branch of the obturator nerve, which can be dissected to a length of 10-12 cm.
During the second-stage procedure, the surgeon must identify the distal end of the nerve graft and send a frozen section for confirmation of viable axons. The muscle flap is harvested and transferred to the face. The flap is secured to the periosteum of the zygomatic arch and the modiolus in a vector that corresponds to the smile on the contralateral face. Subsequently, the microanastomosis between the flap and recipient vessels is executed, followed by the nerve anastomosis as close to the muscle as possible. Movement can be expected in 6-9 months, with improvement over the following 2-3 years.
Lifchez and Gasparri endorse the serratus anterior for free-muscle transfer based on their anatomical findings.13 Each serratus slip, divided along fascial planes, can generate a distinct force vector for facial reanimation with a total of 5 slips and 10 subslips. This serratus anterior can, therefore, be used as a single donor muscle with multiple vectors of action and multiple functions (eg, restoration of a symmetric smile with simultaneous but independent eyelid closure).
Terzis and Noah found no significant effect of age, gender, or ischemia time on outcome in their series of 100 free-muscle transfers.14 They report moderate or better results in 80% of patients undergoing free-muscle transfer, based on a 5-step scale of judgment. O'Brien et al report good-to-excellent results in 51% of 47 patients treated by microvascular free-muscle transfer; the surgeons most commonly used cross-facial nerve grafts and gracilis muscle transfers in their technique.15
One-stage free muscle transfer
In their study of 25 patients, Kumar and Hassan compared single-stage versus dual-stage free tissue transfer for facial reconstruction.16 The gracilis obdurator nerve branch can yield a length of 12 cm, which allows primary anastamosis of this nerve to the contralateral facial nerve. However, this technique produces an additional scar on the cheek. The single-stage transfer has fewer complications and a reduced recovery time with decreased rehabilitation, but the dual-stage approach has overall better symmetry.
In their investigation of 166 free gracilis transfers, Manktelow and Zuker explored muscle transfer with cross-facial nerve graft versus single-stage transfer to the masseter nerve. The excursion of the free gracilis innervated by the masseter nerves is greater than that of the cross-facial nerve graft. This is probably attributable to the different motor nerve used to reinnervate the muscle. The cross-face nerve graft provides improved spontaneity in terms of movement, which is vital to a normal smile in children. This is a more important characteristic than degree of excursion. Their future studies will explore the nature of spontaneity in their muscle transfers utilizing the masseter nerve as a donor.
Although use of the masseter nerve with free tissue transfer was previously explored and considered only in the setting of M ö bius syndrome, bilateral facial paralysis, and facial paralysis not suitable for cross-facial nerve grafting, the masseter nerves applicability and role has been recently extended to patients with unilateral facial palsy. This one-stage strategy, incorporating the masseter nerve with free tissue transfer, has become a reasonable alternative (and may become the criterion standard) to the dual-stage approach with cross-facial nerve grafting. The enormous advantage of the masseter nerve-free tissue transfer technique is that, unlike the cross-facial nerve, the masseter nerve donor produces a movement and muscle excursion (in relation to smile and commissure excursion) in normal range with consistent movement. Also, this technique obviates the need for a second operation. Mobius Syndrome
Mobius syndrome involves bilateral facial nerve paralysis and can often attack cranial nerves VI, III, and XII. The syndrome generates psychological disability due to lack of facial animation and lack of emotional expression. Patients with immobile faces cannot use their faces to show happiness, sadness, or anger.
The surgical goals for patients with Mobius syndrome are far more modest than and differ from the goals for patients who have unilateral developmental facial paralysis. The restoration of a true smile in these mask-like faces is impossible. Movement can only be restored along one vector. A detailed neurological evaluation can identify possible motor donors or residual function, which can be used for additional dynamic restorations. Because of cranial nerve involvement, a thorough clinical and electrophysiological examination is obligatory.
Most frequently, the reconstructive surgeon performs free tissue transfers with bilateral gracilis muscles anastamosed to the masseter nerves on both sides in order to achieve smile restoration.
After surgery, the rehabilitation of patients with facial paralysis necessitates electromyography (EMG) protocols, behavioral modification, and patient exercises. The patient needs to obtain voluntary control of facial regions. Another adjuvant therapy is the use of percutaneous electrical stimulation to stimulate motor function.
In their patient population of 486 patients and 183 revisions, Takushima and Harii analyzed excessive muscle bulk and dislocation of the transferred free muscle.17 They determined that predicting muscle bulkiness to obtain symmetry of facial contour is difficult during the initial free-muscle transfer. Their study illustrates the wide gamut of revisions, including muscle debulking of cheek, adjusting tension and attachments of transferred free muscle, and lipoinjection to the cheek for better volume symmetry.
The patient with facial paralysis presents a daunting challenge to the reconstructive surgeon. A thorough evaluation, including complete history and careful physical examination, directs the surgeon to the appropriate treatment modality. Dynamic reanimation involves nerve repair, nerve transfer, regional muscle transfer, or free-muscle transfer. None of the procedures can restore all of the complex vectors and balance of facial movement and expression. However, dynamic reconstructive techniques can yield improved facial symmetry, spontaneous and symmetric smile, eye closure and protection, and oral competence, all of which refurbish patients' emotional, psychological, and cosmetic state and disabilities.
facial nerve paralysis, facial paralysis, Bells palsy, Bell palsy, facial denervation, facial reinnervation, dynamic reinnervation, paralyzed face, facial symmetry, facial movement, facial expression, synkinesis, facial nerve symmetry, masseter nerve, single-stage, dual-stage, mobius syndrome, Mobius syndrome, facial nerve, symmetrical smile, facial malignancy, progressive paralysis, progressive facial paralysis, sudden facial paralysis, intracranial nerve, masseter muscle, intratemporal nerve, extratemporal nerve, cross facial nerve graft, facial nerve graft, crossfacial nerve graft, cross-facial nerve graft
Source: Facial Nerve Paralysis, Dynamic Reconstruction: eMedicine Plastic Surgery
No disrespect mkuu lakini upo nje kabisa ya maana halisi ya Kiharusi. What you are talking here is just one of the many pathologies that can occur in Facial nerve. Mind you, lesions in the facial nerve are not synonymous to stroke, na hata kwenye tafsiri yako unasema kiharusi ni ugonjwa wa kupooza upande mmoja, meaning the lesion involves nerves that supply the half of the body, wakati facial nerve only supplies the face, hence the name, facial nerve. However, facial nerve paralysis can as well be a sequelae of stroke.
So, what is kiharusi (stroke)?
In a nut shell, stroke is a medical condition associated with the rapidly developing loss of brain functions that occurs when there is disturbance in the blood supply to the brain.
Disturbances in the blood supply to the brain can either be due to
1. Lack of blood flow to the brain cells (Ischaemia) due to blockage e.g in cases of arterial embolism or thrombosis, or
2. Blood leakage to the brain cells (haemorrhage) e.g. in cases of rupture of berry aneurysm or small brain arteries.
What happens then?
Usually not the whole brain is affected. Cells of the affected area may die and the affected part of the brain may fail to function leading to
1. inability to move one or more limbs on one side of the body (hemiplegia, hemiparesis, kupooza upande mmoja wa mwili au mwili kukosa nguvu upande mmoja)
2. inability to understand a speech
3. Inability to make a speech or articulate words.
3. the patient may be unable to see on one side of the visual field.
The risk factors of stroke include
1. Hypertension (high blood pressure)
3. high cholesterol levels in the diet
4. old age
5. cigarette smoking
6. previous history of stroke or if you have experienced a condition called transient ischaemic attack
7. diseases of the heart affecting its rythm kwa mfano atrial fibrillation
What are the effects of stroke?
Stroke inaweza kusababisha
1. permanent neurological disability kwa mfano kupooza upande mmoja wa mwili, kupoteza uwezo wa kuongea, kusindwa kuona vizuri
2. Complications like pneumonia, infections like UTI
3. Na hata death
What is the management of stroke?
Matibabu ya stroke yanategemeana na aina ya stroke depending on what your investigations will reveal.
1. if the cause of your stroke is blockage of blood vessels due to thrombosis, the doctor may occasionally use drugs generally called antithrombosis. Hizi ni dawa ambazo hutolewa kwa ajili ya kuyeyusha bonge la damu lililoganda na kusababisha mishipa ya damu inayopeleka damu kwenye ubongo kuziba.
In centers with advanced technology, the offending thrombus may be removed directly from the affected cerebral artery by inserting a catheter into the femoral artery directing it into the cerebral circulation to withdraw the clot from the body.
2. if the cause is haemorrhage, the patient may need surgery ambayo hufanywa na neurosurgeons. In most cases, however, the bleeding is self limiting and might not need surgery.
3. As a means of secondary prevention, mgonjwa anaweza kupewa antiplatelet drugs like aspirin au dipyridamole kwa ajili ya kuzuia platelets zisigande kwa hiyo kuleta clots (microemboli), anaweza kupewa dawa za kushusha blood pressure, dawa za kushusha kiwango cha cholesterol (statins) na dawa za kuzuia damu isigande (anticoagulants)
4. The patient will also need rehabilitation to recover lost function, hii inajumuisha physiotherapy (mama cheza), speech therapy, language therapy, au occupational therapy.
Kwahiyo, huwezi kutaja tiba (cure) ya moja kwa moja ya kiharusi isipokuwa mkusanyiko wa tiba mbali (management) kutegemeana na vipimo vinasemaje, sehemu ya ubongo iliyokuwa affected, level of technology involved na aina ya stroke.
What a good expanation! and very usefully... Imeeleweka vema sana.
Just a simple inquiry... Vipi mchango wa emotional factors, psychological au physical shocks ... nafikiri hazina uhusiano wa moja kwa moja labda kupitia risk factor ulizotaja au?
Mkuu Azimio Jipya,
That's a very scientific question/inquiry.
Katika follow-up study moja iliyofanyika kwa miaka 14-year among 2201 middle-aged male study subjects, ilionekana kwamba psychological distress was an independent risk factor for fatal ischemic stroke. In this study, psychological distress was a non-specifical term used to encompass sadness, frustration, anxiety, na hata negative mood states nyingine kadhaa. Ilijumuisha pia mild na severe forms of these mood states, as well as both transient and persistent ones. It also referred to both symptoms of psychiatric disorders and to normal emotional responses to adversity.
Lakini sasa, uhusiano huu wa psychological distress na developing a stroke ni wa moja kwa moja au vipi? Hiyo study ilionesha kuwa, kwa mtu ambaye ni normal and healthy, depression (waliichukulia kama part ya psychological distress) may not contribute to the onset or progression of coronary artery disease. Sababu ni kuwa atherosclerosis (major artery diseases, coronary artery inclusive) hutokea na kuprogress kwa sababu ambazo hazina uhusiano kabisa na depression, isipokuwa basi depression huwa ina-increase risk of cardiac events only kwa mtu ambaye tayari ana coronary artery disease.
Similarly, ilionekana kuwa psychological distress may not promote the development of cerebrovascular disease, but it may instead heighten the risk of fatal stroke in patients with existing cerebrovascular disease.
Kwa hivi kujibu swali lako, ni kweli usababishi wa psychological and emotional factors kwa stroke si wa moja kwa moja bali hupitia kwenye risk factors, na kubwa zaidi ni conditions affecting the cardiovascular system zikiwemo hypertension. Na kuwa uhusiano wa moja kwa moja na mechanism of action kati ya psychological distress and cerebrovascular disease, stroke, and stroke mortality ni kitu ambacho bado kipo under investigation.
Unachakachua vi aya vya wengine bila kutoa marejeo halafu unachomeka vilugha vyako hapa na pale ukidhani utatuzuga wote hapa, wasomi feki wa mitandaoni.
Psychological Distress as a Risk Factor for Stroke-Related Mortality -- Carney and Freedland 33 (1): 5 -- Stroke
LITERATURE MONITOR: RECENT ARTICLES OF INTEREST IN NEUROLOGY
Yes I know its always good to acknowledge ... but to me it was very satifactory, without going into that very long and detailed informations.
Kitu kingine ...inasemekana kuna uhusiano sijui ni wa vipi, but unahusianisha HIV_AIDS na stroke au HBP ... mara nyingi nimefuatia hata mitandaoni but sikupata brief clear explanations..!
Lazima nikiri kwamba nilifanya makosa makubwa kutoku-acknowledge na kerefer literature. Nashukuru kwa kuliona hilo na kunirejesha mstarini. Na nakuomba samahani na kwa yeyote yule kama ulikwazika kwa hilo.
Hata hivyo, kwa mtu anayedhaniwa ni msomi aliyeelimika kumuita mwenzake mwizi mkubwa, sidhani kama ni ustaarabu.
Siko hapa kudefend thesis wala kutaka sifa kwa mtu. Ninachofanya ni kubadilishana mawazo na kupeana elimu ndogo kwa wenye uhitaji. Siyo wote wenye elimu kubwa na uelewa wa medical termonologies kama wewe watakaoelewa kama tukiamua kutumia medical language, kwa hivi lengo lengo la kutumia maneno binafsi ni kufanikisha uelewekaji ingawa kwako imeonekana ni uchakachuaji na machukizo makubwa. Samahani na pole kwa hilo.
Otherwise asante sana kwa reference na natumaini itawasaidia sana wasio na uelewa wa medicine kuelewa vizuri zaidi.
Kama nilikwazika? Kama hujui nilikwazika usiombe msamaha.
"Hata hivyo, kwa mtu anayedhaniwa ni msomi aliyeelimika kumuita mwenzake mwizi mkubwa, sidhani kama ni ustaarabu." Anaedhaniwa na nani? Nani anadhani mimi ni msomi niliyeelimika? Na, unajuaje mimi nakuchukulia wewe kama "msomi aliyeelimika," mtu unaebeba aya nzima nzima unachanganya na lugha yako hapa na pale kuipitisha kama ya kwako? Kuna viwango hapa, ukikwiba ya wengine utaitwa mwizi, usiseme nimekosa ustaarabu, geuka tubu maana nia ya moyo wako imekengeuka.
" Siyo wote wenye elimu kubwa na uelewa wa medical termonologies kama wewe watakaoelewa kama tukiamua kutumia medical language" Umejuaje mimi nina elimu kubwa ya nomino za kiganga?
Asante kwa kunikumbusha umuhimu wa kuacknowledge. Nimekupata vema.
Turudi kwenye mada yetu,
Ni kweli kuna uhusiano mkubwa kati ya HIV-AIDS na kiharusi. HIV/AIDS inaongeza uwezekano wa kupata kiharusi hata kwa wagonjwa ambao hawana zile risk factors nyingine za kupata stroke au wale ambao risk factors zao tayari zipo controlled.
Tunafahamu kuwa HIV-AIDS huwa inaleta magonjwa nyemelezi mengi sana na hivi kuathiri karibu kila mfumo wa mwili. Mojawapo ni yale yanayohusiana na mfumo wa fahamu na yale yanayoweza kuathiri ubongo kwa mfano Toxoplasmosis. Kwa hiyo inapotokea zile tando zinazouzunguka mfumo wa fahamu (meninges) zikawa infected na haya magonjwa nyemelezi kama cryptococcal meningetides, hali hii hupelekea kuathirika kwa hizo tando (meningitis) na hivyo kuongeza uwezekano wa kutokea kiharusi. Wakati mwingine magonjwa hayo nyemelezi huweza kushambulia moja kwa moja mishipa midogo ya damu inayopeleka damu katika ubongo (vasculitides) na hivyo kusabisha uwezekano wa kupata kiharusi kwa ama mishipa hii kuziba (ischaemic stroke) au kupasuka (haemorrhagic stroke) kwa sababu ya kuwa dhaifu na kushindwa kuhimili shinikizo la damu ndani yake.
Wakati mwingine hutokea mgonjwa wa HIV-AIDS akapata TB inayoweza kusambaa mpaka kwenye ubongo na kusababisha kitu kinachoitwa (Tuberculoma) au anaweza kupata Toxoplasmosis. Vyote hivi huwa na tabia ya kutengeneza kitu kinachoitwa Space Occupying Lesions (SOL) ambazo hupunguza mtiririko wa damu kwenda katika eneo husika la ubongo na hivi kupelekea mtu mwenye HIV-AIDS kupata kiharusi.
Namna nyingine ni kuathirika kwa mishipa ya damu inayopeleka damu kwenye ubongo baada ya kushambuliwa moja kwa moja na HIV au matokeo yake, na hivyo kufanya mtiririko wa damu kwenda kwenye ubongo uathirike kwa kiasi kikubwa.
Maelezo zaidi ya mechanisms nyingine gonga hapa Mechanisms of ischemic stroke in HIV-infected patients -- Ortiz et al. 68 (16): 1257 -- Neurology na hapa http://stroke.ahajournals.org/cgi/content/full/27/3/538
Tiba ya huo ugonjwa wa Kiharusi ni ngumu kutibika .
Kiharusi ni ugonjwa mkali wa mishipa ya damu kwenye ubongo unaohatarisha vibaya afya na maisha ya binadamu. Takwimu husika zimeonesha kuwa, kila mwaka watu milioni 1.5 wanapatwa na ugonjwa huo nchini China, na nusu kati yao wanakufa kutokana na ugonjwa huo, na watu wengi wanaopona wanapoteza uwezo wa kufanya kazi kwa viwango tofauti. Hali hiyo imesababisha mzigo mkubwa kwa familia na jamii.
Mzee Wang Qinmei mwenye umri wa miaka 65 ana afya njema na hakuwahi kupatwa magonjwa makubwa. siku moja asubuhi katika majira ya mchipuko mwaka huu, alienda sokoni kwa baisikeli kununua chakula kama kawaida, ghafla alijisikia kizunguzungu na akapoteza fahamu. Baada ya muda mfupi, alipata fahamu na kuomba msaada kutoka kwa wapita njia na akapelekwa hospitali.
Katika chumba cha huduma ya kwanza, daktari alithibitisha haraka ugonjwa uliompata mzee Wang. Daktari wa upasuaji wa mishipa ya damu kwenye ubongo katika hospitali ya 301 ya jeshi la ukombozi wa watu wa China Bw. Wang Jun alisema:
"baada ya kumfanyia upimaji wa CTA, tuligundua sehemu moja nyembamba katika mishipa mikubwa ya damu iliyoko shingoni, na asilimia 90 ya sehemu hiyo ya mishipa ya damu imezibwa. Hali hiyo ni ya hatari sana."
Tatizo la wembamba wa mishipa ya damu ya shingoni ni chanzo kikubwa cha ugonjwa wa kiharusi wa aina ya kukosa damu kwenye ubongo. Asilimia 60 ya wagonjwa wa ugonjwa huo wanatokana na tatizo la kuzibwa kwa mishipa ya damu ya shingoni. Pamoja na kuzidi kuziba kwa mishipa ya damu, dalili za ugonjwa huo zinaonekana kidhahiri na wazi zaidi, hatimaye zinasababisha kiharusi kibaya. Kwa kuwa asilimia 90 ya mishipa ya damu ya shingoni inakuwa imeziba, hali hiyo inaufanya ubongo ukose damu na oksijen, na dalili mbalimbali za ugonjwa huo zote zinasababishwa na tatizo hilo.
Mbali na kiharusi cha kukosa damu kwenye ubongo, aina nyingine ni kiharusi cha kutokwa damu kwenye ubongo. Chanzo kikubwa ni shinikizo kubwa la damu linalosababisha mishipa midogo ya damu kwenye ubongo ivimbe na kupasuka.
Kwanza, ugonjwa wa kiharusi unahusiana na umri na jinsia. Kwa kawaida, watu wenye umri wa zaidi ya miaka 55 wana hatari kubwa zaidi ya kupatwa na kiharusi, na hatari ya kupatwa ugonjwa huo kwa wanaume ni asilimia 50 zaidi kuliko wanawake. Ya pili, ugonjwa huo ni wa kurithi. Aidha, magonjwa ya shinikizo kubwa la damu, kisukari, tatizo la moyo, tatizo la kuwa na uzito kupita kiasi, kuvuta sigara na kunywa pombe zote zinaweza kusababisha kiharusi.
Kwa kawaida, kuna dalili kadhaa zinaonekana kabla ya kutokea kwa kiharusi. Mkurugenzi wa idara ya upasuaji wa mishipa ya damu katika hospitali ya 301 ya jeshi la China Bw. Li Baomin alisema:
"kabla ya kutokea kwa kiharusi, mgonjwa hujisikia kizunguzungu, mwasho kwenye mikono na miguu, na kutoona vizuri. Baada ya muda, hisia hiyo itaisha au itarejea tena. Kama una dalili hizo, ni lazima uchukue tahadhari."
Bw. Li alisema, kama dalili hizo zinatokea mara kwa mara katika siku moja au mbili, na pia una shinikizo kubwa la damu au ugonjwa wa kisukari au ugonjwa wa kurithi, unapaswa kwenda hospitali mara moja kufanyiwa uchuguzi. Hivi sasa, ugonjwa wa kiharisi unaweza kuthibitishwa mapema na kwa usahihi.
Basi kama wagonjwa wakipatwa na kiharusi nyumbani au kwenye sehemu za hadhara tutafanyaje? Watalaamu wanaeleza kuwa, kiharusi kinatokea ghafla, wagonjwa wanaweza kupoteza fahamu, kuanguka, kutikisika au kushindwa kuongea. Watu huchanganyikiwa wakati hali hiyo ikitokea, na hata wanakuwa hawajui la kufanya. kwa kawaida, watawaamsha hata kuwatingisha wagonjwa. Vitendo hivyo vinaweza kuwadhuru wagonjwa hao, hata vinafanya hali yao iwe mbaya zaidi.
Kama mtu akipatwa kiharusi, kwanza jamaa zake wasihangaike, bali wanatakiwa kumtuliza mgonjwa, na ni afadhali wasimwamshe alipo, lakini wanatakiwa kumwita daktari mara moja. na ni bora walegeze nguo za ndani za mgonjwa, hatua hiyo inamsaidia mgonjwa kupumua bila tatizo. Kama mgonjwa akitikisika, hali hiyo ni mbaya, ni lazima wamshtue. Kwa kuwa wakati huo, mgonjwa anaweza kujiuma ulimi, hivyo ni afadhari wazibe mdomo wa mgonjwa kwa nguo. Wagonjwa wengi wa kiharusi wanatapika, ili kuzuia wagonjwa kama hao wasijizibie koo, ni bora kuwalaza shingo upande. Kama matapishi yakibaki mdomoni, ni lazima yatolewe mdomoni kwa vijiti, na kama mgonjwa huyo ana meno bandia, inapaswa kuyatoa ili yasije yakaingia kooni.
Zamani ugonjwa wa kiharusi ulikuwa unatibiwa kwa upasuaji, hivi sasa unatibiwa kwa matibabu yenye usalama, ufanisi na rahisi zaidi. Matibabu hayo ni kuingiza mrija mdogo kwenye mshipa mkubwa wa damu wa pajani na kuifikisha kwenye sehemu yenye tatizo mwilini na kutibu. Kwa kuwa kipenyo cha mshipa mkubwa wa damu ni milimita 15 hivi, na kipenyo cha mirija ni milimita 2 tu, hivyo mrija huo unaweza kupita kwenye mishipa ya damu bila tatizo. Mbali na hayo, kutokana na kuwa hakuna nevu za hisia ndani ya mishipa ya damu, basi wagonjwa hawasikii maumivu.
Mzee Wang Qinmei alitibiwa kwa matibabu hayo. Daktari aliweka chombo maalum cha kupanua mshipa wa damu ndani ya sehemu ya mshipa mkubwa wa damu wa shingoni kwake iliyozibwa kwa kutumia mirija. Mzee Wang alisema:
"Baada ya kuwekewa chombo cha kupanua mshipa wa damu, nilisikia damu inapita vizuri, ghafla hisia ya kizunguzungu iliondoka mara moja."
Matibabu hayo hayahitaji kuwapa wagonjwa nusukaputi ya mwili mzima. Wagonjwa wanaweza kutibiwa wakiwa na fahamu vizuri. Pia kwa kuwa matibabu hayo yanaleta majaraha madogo tu, basi wagonjwa wanaweza kutembea saa 24 tu baada ya matibabu. Hivi sasa, wagonjwa wengi zaidi wa kiharusi wanachagua matibabu hayo.
Tuko pamoja mkuu!
Sikuona mahali ulipo gusia Moyo kuathirika moja kwa moja kwa virusi vya ukimwi kama inavyoweza kuwa kwa ubongo wenyewe.
Nafikiri wakati Rais Nigeria alipokuwa mgonjwa anaumwa na maradhi ya Moyo ... etc, nilisikai Dr mmoja akielezea posibilities. Moja, alitaja kuwa ni uwezekano wa infection ya HIV kwenye utando fulani wa Moyo!
Mzimzi mkali where are you!!