Ugonjwa wa kiharusi/ kupooza (stroke): Kinga, tiba na jinsi ya kukabiliana na maradhi haya

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Nov 9, 2006
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MARADHI YA KIHARUSI
Kiharusi ni hali inayotokea pale mishipa inayosambaza damu kwenye ubongo inapopatwa na misukosuko kiasi cha kushindwa kupeleka damu kwenye ubongo na hivyo kuathiri ufanyaji kazi wa ubongo kwa zaidi ya masaa 24.

Kulingana na shirika la afya duniani kiharusi ni nakisi katika neva ambayo hutokana na tatizo katika mishipa ya damu ya ubongo na ambalo huendelea zaidi ya masaa 24 au kukoma ndani ya masaa 24. Muda wa masaa 24 umechukuliwa ili kutofautisha kiharusi na kiharusi cha kukosa oksijeni katika ubongo (ischemia) ambacho hutokea na kudumu kwa muda mfupi yaani (transient ischemic attack).

Kwa kawaida dalili za TIA hupotea na mtu kurudia hali yake ya kawaida ndani ya masaa 24.
webmd_rm_illustration_of_stroke_causes_.jpg



Aina za kiharusi
Kiharusi kimegawanyika katika aina kuu mbili kulingana na jinsi kinavyotokea (visababishi vyake). Aina hizo ni:

1. Kiharusi cha kukosa hewa kwenye Ubongo (Ischemic stroke)

Aina hii ya kiharusi hutokea iwapo usambazaji wa damu katika sehemu ya ubongo hupungua na kupelekea tishu za ubongo za eneo liliathirika kushindwa kufanya kazi zake vizuri.

Aina hii ya kiharusi husababishwa na nini?

Aina hii ya kiharusi husababishwa na damu iliyoganda kuziba mishipa midogo ndani ya ubongo (cerebral thrombosis) au Kipande cha damu kumeguka na kwenda kuziba mshipa wa damu kwenye ubongo(cerebral embolism)

Kupungua kwa usambazaji wa damu kwa ujumla kwa mfano shock.
Vena thrombosis.

2. Kiharusi cha kuvuja damu ndani ya Ubongo (Haemorrhagic Stroke)
Aina hii ya kiharusi hutokea pale ambapo mishipa midogo ya damu ndani ya ubongo hupasuka na kusababisha kusambaa kwa damu ubongoni (cerebral hemorrhage). Mara nyingi aina hii ya kiharusi hutanguliwa na dalili za kichwa kuuma, au kuwepo kwa historia ya ajali ya kichwa.

Visababishi vya Kiharusi (kwa ujumla)
- Wakati fulani, mishipa ya damu huzungukwa na aina fulani za mafuta yasiyofaa mwili, hali inayoitwa kitaalamu kama atherosclerotic plaque. Hali hii husababisha kuganda kwa damu katika

- mishipa (thrombosis) hiyo. Kuganda huku kwa damu kunaweza kutokea kwenye mishipa mikubwa au midogo inayopeleka damu kwenye ubongo. Baadhi ya mishipa mikubwa ya damu inayoweza

- kuathirika na tatizo hili ni pamoja na arteri za common carotid na interior carotid arteries, na arteri za vertebral. Nyingine ni mishipa midogo inayounda eneo linaloitwa circle of willis lililo katika ubongo.

- Kuganda kwa chembe nyekundu za damu za mgojwa wa sickle cell kunaweza pia kusababisha kuziba mishipa ya damu hivyo kusababisha Kiharusi.

- Kuganda kwa damu (embolus) kwenye mishipa ya damu ya sehemu nyingine za mwili au (hewa, mafuta, kusanyiko la vijimelea kama bakteria waletao ugonjwa wa endocarditis) huweza

- kusababisha kuziba kwa mishipa inayosambaza damu kwenye ubongo na hivyo kusababisha kiharusi.

- Upungufu wa usafirishaji damu mwilini (systemic hypoperfusion) - Wakati fulani moyo hushindwa kusukuma damu vizuri kwenda sehemu mbalimbali za mwili ikiwemo ubongo kutokana na kufa kwa

- sehemu za nyama ya moyo kwa kukosa damu ya kutosha (Ischaemic Heart Diseases) au kutokana na kujaa kwa maji kwenye gamba lake la nje (pericardial effusion) au kupungua kwa damu mwilini,

- kunakoweza kusababishwa na mambo kadhaa. Hali hii husababisha sehemu kubwa ya mwili ikiwemo ubongo kukosa oksijeni ya kutosha na kusababisha kuathiriwa kwa sehemu ya ubongo.

- Shinikizo la damu la muda mrefu lisilothibitiwa linaweza kusababisha kupasuka kwa mishipa midogo inayosambaza damu kwenye ubongo na hivyo damu kujaa kwenye ubongo (Intracerebral hemorrhage).

Dalili za kiharusi
Dalili za kiharusi hutegemea na eneo la ubongo liliathiriwa.

- Iwapo sehemu ya ubongo mkubwa ( Cerebellum) itaadhirika, mgonjwa atakuwa na dalili kama kushindwa kutembea vizuri, hivyo kuathiri mwendo wake, kujihisi kizunguzungu na pia kutapika.

- Iwapo sehemu ya ubongo wa kati (cerebral cortex) itakuwa imeathirika, mgonjwa atakuwa na dalili za kushindwa kuongea,kushindwa kuelewa lugha inayozungumzwa, kushindwa kuona vizuri, kuwa

- na ukosefu wa kumbukumbu, kuwa na mvurugiko wa mpangilio wakw wa kufikiri, kuchanganyikiwa, na kubadilika kwa mwendo wa harakati za hiari.

- Iwapo mgonjwa ataadhirika sehemu ya ubongo kwenye shingo kuelekea kwenye uti wa mgongo (brain stem), mgonjwa anaweza kuwa na dalili za kuhisi mabadiliko ya harufu, ladha, kusikia na

- kuona; kulegea kwa misuli ya macho (ptosis); kupungua kwa ufahamu na kulegea kwa misuli ya uso; Ulegevu wa Ulimi (kushindwa kutoa nje au kusogeza upande upande); kupungua uwezo wa

- kumeza; ulegevu wa misuli ya shingo na kushindwa kugeuza shingo upande mmoja; kushindwa kusimama sawasawa na kuona vitu kwa hali ya utofauti; mabadiliko ya upumuaji na kiwango cha moyo kudunda.

- Iwapo sehemu mojawapo ya mfumo mkuu wa neva (central nervous system) imeathirika, mgonjwa atakuwa na dalili za kupoteza ufahamu kwa upande mmoja wa mwili na kulegea kwa misuli ya uso, kuhisi ganzi mwilini, na kupungua kwa ufahamu wa hisia na hisia mtetemo.

- Aidha bila kujalisha eneo lililoathiriwa, mgonjwa pia anaweza kuwa na dalili za kupoteza fahamu, maumivu makali ya kichwa na kutapika. Dalili hizi za kuumwa kichwa na kutapika kwa kawaida

- hutokea kwa mgonjwa mwenye kiharusi cha kuvuja damu (hemorrhagic stroke) ambacho husababisha ongezeko la shinikizo na mgandamizo wa ubongo ndani ya fuvu kutokana na kuvuja kwa damu.


Vipimo
  • Mionzi
  • CT-scan
  • MRI
  • PET
  • SPECT
Vipimo vingine ni;
ECG, ECHOCARDIOGRAM huwezesha kutambua hitilafu katika mapigo ya moyo (arrhythmia) na kama kuna damu iliyoganda kwenye moyo ambayo inaweza kufika kwenye ubongo

Holter monitor husaidia kutambua hitilafu katika mapigo ya moyo (arrhythmia) zinazotokea kwa vipindi

Angiogram huwezesha kugundua matatizo kwenye mishipa ya damu, na ni mishipa ipi ya damu iliyoziba.
Vipimo vya damu huwezesha kutambua uwepo wa lijamu mwilini (hypercholesterolemia) na mabadiliko mengine katika damu
Vihatarishi vya kiharusi

Vitu vinavyoweza kumuweka mtu katika hatari ya kupata kiharusi ni pamoja na

  • Shinikizo la damu lisilothibitiwa
  • Kisukari
  • Uvutaji sigara
  • Unywaji pombe kupita kiasi
  • Kutofanya mazoezi kabisa
  • Fetma (obesity)
  • Kuwa na cholesterol nyingi kwenye damu
  • Atrial fibrillation
Matibabu
Matibabu ya kiharusi hutegemea pia aina na visababishi vyake .

1. Matibabu ya kiharusi kinachotokana na ubongo kukosa hewa (Ischemic stroke)

Mgonjwa hutibiwa kwa kutumia dawa za kuyeyusha damu iliyoganda (thrombolytics) au kwa kuondoa damu iliyoganda kwa njia mbalimbali (thrombectomy). Dawa nyingine kama vile junior Aspirin na Clopidogrel hutolewa kwa ajili ya kuzuia chembe sahani kukusanyika na kuganda.

2. Matibabu ya kiharusi kinachotokana na damu kuvujia kwenye ubongo (Hemorrhagic stroke)

Aina hii ya kiharusi huitaji tathmini ya upasuaji wa neva ili kuchunguza na kutibu sababu ya damu kuvuja. Angalizo: ni hatari kumpa mgonjwa wa aina hii ya kiharusi dawa za kuyeyusha damu

iliyoganda au za kuzuia kuganda maana uhatarisha maisha ya mgonjwa badal ya kumsaidia. Kwahiyo ni vizuri kwa wataalamu kufanya ufanya uchunguzi wa kutosha ili kuwa na uhakika na tatizo.

Huduma na Matunzo kwa mgonjwa wa Kiharusi

Mojawapo ya mambo muhimu ya kufanya kwa mgonjwa aliyepata kiharusi ni kumuongoza na kumuelimisha ili arudishe ujuzi wake wa maisha ya kila siku. Hapa uhitaji ushirikiano wa wauguzi,

wataalamu wa viungo, wataalamu wa ushauri wa kazi na daktari. Kuna umuhimu pia wa kuwaelimisha ndugu kuhusu hali ya mgonjwa ili waweze kumsaidia katika matunzo yake nyumbani na kwenye jamii inayomzunguka.

Matarajio (prognosis)

Asilimia 75 ya wagonjwa wa kiharusi wanaonusurika kifo huwa walemavu na kusababisha kuathirika kwa ufanyaji kazi wao na kuajiriwa. Ulemavu unaweza kuwa wa kimwili au kiakili au vyote kwa pamoja.

Ulemavu wa kimwili ni pamoja na

- Ulegevu wa misuli
- Kujihisi ganzi sehemu mbalimbali za mwili hususani zilizoathirika
- Kujikojolea
- Kutoona vizuri
- Kushindwa kuendelea na shughuli za kila siku
- Vichomi
- Vidonda shinikizo
- Kukosa hamu ya chakula.
- Ulemavu wa akili hujumuisha vitu kama
- Mgonjwa kuwa na wasiwasi
- Hofu ya mashambulizi, na
- Unyongovu.

Jinsi ya kuzuia kiharusi
- Zuia au tibu shinikizo la damu
- Dhibiti kisukari
- Fanya mazoezi
- Acha kuvuta sigara
- Punguza uzito
- Acha kunywa pombe kupita kiasi
- Tumia Junior Aspirin
- Kula chakula kisichokuwa na mengi na kisicho na chumvi nyingi.
- Tumia dawa za kupunguza mafuta mwilini (statins)kwa mfano Simvastatin
===
What Is a Stroke?

Stroke is a medical emergency and a leading cause of death in the U.S. It occurs when a blood vessel in the brain bursts or, more commonly, when a blockage develops. Without treatment, cells in the brain quickly begin to die. The result can be serious disability or death. If a loved one is having stroke symptoms, seek emergency medical attention without delay.
getty_rm_illustration_of_stroke.jpg


Stroke Symptoms

Signs of a stroke may include:

  • Sudden numbness or weakness of the body, especially on one side.
  • Sudden vision changes in one or both eyes, or difficulty swallowing.
  • Sudden, severe headache with unknown cause.
  • Sudden problems with dizziness, walking, or balance.
  • Sudden confusion, difficulty speaking or understanding others.
Call 911 immediately if you notice any of these symptoms.

phototake_rm_photo_of_brain_damage_from_stroke.jpg


Stroke: Time = Brain Damage
Every second counts when seeking treatment for a stroke. When deprived of oxygen, brain cells begin dying within minutes. There are clot-busting drugs that can curb brain damage, but they have

to be used within three hours of the initial stroke symptoms. Once brain tissue has died, the body parts controlled by that area won't work properly. This is why stroke is a top cause of long-term disability.
 
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???to The best of my KNOWLADGE harusi hushangiliwa kwa kupungiwa mikono,.na wengine hunyanyua miguu...wagonjwa ni wengi,.....

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


Introduction

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:



  1. Facial symmetry at rest
  2. Symmetrical smile
  3. Voluntary, coordinated, spontaneous facial movements
  4. Oral competence and eyelid closure with corneal protection
  5. 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

History

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.

Physical


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
.

Diagnostic Studies


Audiometry

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.

Radiography


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.

Nerve Repair

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:


  1. The number of axons remaining in the nerve
  2. The potential for regeneration of axons
  3. 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

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

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

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.

Techniques

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.

Muscle Transposition

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.

Temporalis

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.

Masseter

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.

Digastric

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 nerve’s 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.

Follow-up

Rehabilitation
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.

Revisions

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.

Summary

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.

Keywords


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
 
MziziMkavu,


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)
2. Diabetes
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.
 
KARDINALI!

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?
 
KARDINALI!

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.
 
Kardinali,

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..!
 
… Na nakuomba samahani na kwa yeyote yule kama ulikwazika kwa hilo.
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?
 
Kardinali,

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..!

Azimio Jipya,
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 [URL="http://stroke.ahajournals.org/cgi/content/full/27/3/538http://www.neurology.org/cgi/content/abstract/68/16/1257"]http://stroke.ahajournals.org/cgi/content/full/27/3/538[/URL]
 
Kardinali,

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.





0905.jpg
 
Kardinali:

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!
 
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.

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Mungu akusidishie MziziMkavu, kwa maelekezo yako ya tiba pamoja na tiba zako za asili.
Wengi zimetusaidia
Asante sana na wewe pia akuzidishie Mungu kila la kheri sisi Mwenyeezi Mungu alituumba tuwe tunawasaidia watu wengine kimawazo,kidawa, kifikiria na kila kitu bila kuhitaji kitu chochote zaidi ya dua zenu tu. Ingawa sisi wengine hatujakwenda chuo kikuu

lakini mwenyeezi Mungu ametupa talent Vipaji vya kuwasaidia watu Tangu mwaka 1980 nilikuwa naweza kuwasaidia wengi tu na pia nina kipaji cha kuweza kumsoma mtu uso wake yaani psikoloji, saikoloji na kumjuwa huyu mtu ana matatizo gani na njia gani aweze kuifanya ili matatizo yake yamuondokee nina mambo mengi tu lakini machache ni hayo asante sana Mkuu ubarikiwe.
 
Wakati wa sherehe msichana mmoja kwa mashaka na alianguka. Aliombwa aitiwe ambulance, lakini yeye alimwakikishia kila mtu kuwa kila kitu ni sawa na kwamba yeye kajigonga kwa sababu tu ya viatu vipya.
Kwa vile alionekana kuwa na wasiwasi na kuwa anatetemeka kidogo, walimsaidia kumfuta na kumpatia maji ya kunywa. Siku yote baadae msichana huyu aliendelea vizuri na kuonenekana kidogo mwenye furaha. Baadae mume wa msichana amlipigia simu kila kila mtu na kusema kuwa mkewe alikuwa kapelekwa hospitali na Saa 23:00 alifariki. Katika sherehe ile yule msichana alishikwa na kiharusi (acute ischemic stroke)
Kama watu waliokuwa katika sherehe ile wangelijua jinsi ya kuangalia ishara za kiharusi,yule msichana angaliweza kuwa bado anaishi.
Baadhi ya watu baada ya kupata ugonjwa huu wa kiharusi hawafi hapo hapo. mara nyingi wanakutwa katika hali ambayo wanaweza saidiwa au hata kujisaidia wenyewe.
Huu hapa ni ushauri wa kufanya ili kumsaidia mtu nayepatwa ka kiharusi.

Daktari husema kwamba kama ni ndani ya saa 3 tangu mwathirika wa kiharusi hapate hizo dalili, matokeo ya mashambulizi yanaweza kuondolewa. Kitu cha muhimu ni kugundua na kutambua kiharusi na kuanza matibabu ndani ya masaa ya kwanza 3 - ambayo kwa hakika si rahisi wengi wetu.

Kutambua kiharusi: Kuna njia 4 za kutambua kiharusi.

- Uliza mtu kutabasamu (atashindwa kutabasamu)

- Uliza kusema sentensi rahisi (kwa mfano "Leo hali ya hewa ni nzuri")

- Mwulize kuinua mikono miwili (hawawezi au nusu tu na uwezo wa kuchukua)

- Mwulize kuweka nje ulimi (kama ulimi umeeleka upande mwingine an haurudi sawa hiyo pia ni dalili ya kiharusi.)

Kama matatizo haya yanajitokeza, na hata kama ni dalili moja kati ya hizo hapo juuni vema kwa haraka zaidi kumpeleka mgonjwa hospitalini, au kama kuna uwezekano ita ambulance.

ukituma ujumbe huu katika sehemu au kwa watu kumi unaweza okoa maisha ya watanzania wengi.
 
Asante kwa kunifunua macho,kwani nilishawahi kuona mama mmoja anafariki kwenye gari bila kujua nini tatizo,baadae alikuja mtaalam akasema alipatwa na kiharusi....
 
Asante; je chance ya kupona kwa watu waliopata stroke ikoje. Kupona nikiwa na maana ya kutokufa, hata kama atakuwa mlemavu?
 
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