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[Facial paralysis in children].

Facial paralyses in children may be grouped under headings displaying a certain amount of individuality. Chronologically, first to be described are neonatal facial paralyses. These are common and are nearly always cured within a few days. Some of these cases are due to the mastoid being crushed at birth with or without the use of forceps. The intra-osseous pathway of the facial nerve is then affected throughout its length. However, a cure is often spontaneous. When this desirable development does not take place within three months, the nerve should be freed by decompressive surgery. The special anatomy of the facial nerve in the new-born baby makes this a delicate operation. Later, in all stages of acute otitis, acute mastoiditis or chronic otitis, facial paralysis can be seen. Treatment depends on the stage reached by the otitis: paracentesis, mastoidectomy, various scraping procedures, and, of course, antibiotherapy. The other causes of facial paralysis in children are very much less common: a frigore or viral, traumatic, occur ring in the course of acute poliomyelitis, shingles or tumours of the middle ear. To these must be added exceptional causes such as vitamin D intoxication, idiopathic hypercalcaemia and certain haemopathies.

Adolescent↗

[Facial paralysis and tuberculous otitis. Significance of early neural decompression].

Facial paralyses associated with tuberculous otitis have consistently had a bad prognosis. This is bound up with delay in diagnosing the tuberculous nature of the lesions and with slow-acting medical treatment. The facial nerve must be decompressed immediately and not delayed until medical treatment has failed. This attitude is particularly necessary in two types of circumstances in which the tuberculous origin should be under suspicion as a matter of routine / firstly when facial paralysis appears in the secondary sequelae of ear surgery and, secondly, when facial paralysis is a complication in chronic otitis without cholesteatoma.

Adult↗

[Laser posterior cordectomy in bilateral vocal cord paralysis].

OBJECTIVES: We evaluated the functional results of laser posterior cordectomy with respect to respiration, phonation, and deglutition. PATIENTS AND METHODS: Unilateral laser posterior cordectomy was performed in nine patients (7 women, 2 men; mean age 56 years; range 46 to 61 years) with bilateral vocal cord paralysis. Postoperatively, respiration, deglutition, and phonation were evaluated with the use of an exercise tolerance scale, the Pearson scale, and wavelet analysis, respectively. The mean follow-up period was 14.2 months. RESULTS: Respiration was satisfactory in eight patients. Of these, four patients had excellent, and four patients had good exercise tolerance. The procedure resulted in success without tracheotomy in four patients. No deglutition or aspiration problems developed. Of eight patients with satisfactory respiration, voice quality remained unchanged in six patients, whereas an improved voice quality was noted in two patients who received postoperative phoniatric rehabilitation. CONCLUSION: Laser posterior cordectomy for the treatment of bilateral vocal cord paralysis resolves respiration problems, it restores phonation and deglutition functions, as well.

Deglutition↗

[Acute flaccid paralysis after drug injection: a case report in the pediatric service of the Befelatanana Hospital Center in Antananarivo].

In the framework of the poliomyelitis program eradication, the World Health Organization suggests two markers to survey the circulation of the poliovirus: notification of all cases of acute flask paralysis (AFP) and etiological research of these AFP from two stool samples. The authors reported the case of a AFP, occurring after a polio vaccination in a 5-year-old boy who had later an acute rhinopharyngitis treated by antibiotics and quinine intramuscular injections. A left lower limb AFP justified his hospitalisation. The isolation of a Sabin type 3 poliovirus was a pitfall because clinical and complementary investigations demonstrate a peripheral neuromuscular paralysis. This demonstrative case shows the need for health staff to be trained to perform correctly an usual act like intramuscular drug injections.

Acute Disease↗

[Bilateral phrenic nerve paralysis, dysautonomia and restrictive cardiomyopathy in a case of POEMS syndrome].

We report a case of POEMS syndrome (Polyneuropathy, Organomegaly, Endocrinopathy, M protein and Skin changes) with unusual clinical features. A 62-year-old woman presented a severe polyneuropathy with dysphonia and vegetative symptoms, including bradycardia and sphincterial disorders. The clinical examination showed facial hyperpigmentation, cachexia, anasarca and splenomegaly. She also presented restrictive cardiomyopathy and endocrine disturbances. Nerve conduction studies revealed a severe demyelinating sensorimotor neuropathy. Cerebrospinal fluid analysis showed an elevated protein level. We detected a biclonal gammapathy (Ig G and Ig A with lambda light chain) and lytic pelvic bone lesions. Later, she developed a severe ventilatory failure due to a bilateral phrenic nerve paralysis leading to a mechanical ventilation. Steroids followed by localized radiotherapy partially improved the respiratory status and stabilized the neuropathy. Phrenic nerve paralysis, restrictive cardiomyopathy, vegetative symptoms and cranial nerve palsy are exceptional in POEMS syndrome. Moreover, this case emphasizes the importance of radiological investigations since the discover of plasmocytoma may improve the prognosis of POEMS syndrome.

Anti-Inflammatory Agents↗

[A case of Gitelman's syndrome presenting with the hypokalemic periodic paralysis].

We report a rare case of Gitelman's syndrome (GS) presenting with the hypokalemic periodic paralysis. A 27-year-old man was admitted to our hospital because of transient weakness of the limbs. Past history was unremarkable, including the delivery and early developmental milestones, except for a transient limb weakness 7 times since the age of 15 years. The blood pressure was 140/90 mmHg. The physical examinations were unremarkable. Neurologically, the patient was fully oriented. The cranial-nerve functions were intact. Manual muscle tests revealed 1/5 weakness in his neck and extremities. Sensation was normal in all modalities. The deep tendon reflexes were present but decreased mildly. Laboratory tests showed hypokalemia (1.9 mEq/l), hypomagnesemia (1.8 mEq/l), and hypocalciuria (40.0 mg/dl). Plasma rennin activity and aldosterone concentration were elevated. The molar ratio of urinary calcium/creatinine was 0.11 (< 0.2). Arterial blood gas showed mild metabolic alkalosis with respiratory compensation. Because of these data, the diagnosis of GS was made. Gene mutations in the renal thiazide sensitive Na-Cl cotransporter (TSC) have already been shown to cause GS. Although we searched for gene mutation of TSC, none of 25 mutations in 18 out of 26 exons which had been previously reported were found. This is the first report of Gitelman's syndrome presenting with the hypokalemic periodic paralysis in Japan.

Adult↗

Surgical reconstruction of irreversible ulnar nerve paralysis in leprosy.

Twenty-five patients with irreversible leprotic ulnar nerve palsy having undergone lumbrical replacement with two different tendon transfer techniques were assessed 6-120 months after surgery. Nineteen patients were reconstructed with the flexor digitorum four-tail procedure (FDS-4T), and six with Zancolli's lasso procedure (ZLP). Mean paralysis times were 103 months for FDS-4T, and 68 months for ZLP. Mean age of the patients was 36 years (21-57). Grip strength measurements, improvement in active range of motion at the PIP joints, patients' ability to open and close their hands fully, as well as sequence of phalangeal flexion, were noted. Mean grip strength measurements during follow-up were 76% of the contralateral extremity in the FDS-4T group and 82% in the ZLP group. Comparison of the follow-up grip strength with the preoperative value revealed 1% improvement in the FDS-4T group and 20% in the ZLP group. Claw hand deformity was completely corrected in 12 patients in FDS-4T group, and in five patients in the ZLP group. Residual flexion contracture remained in five patients after surgery. Swan-neck deformity subsequently developed in seven fingers. Age, sex, mean follow-up and surgical technique did not relate statistically to the functional outcome. However, preoperative extensor lag of the PIP joint and mean paralysis time significantly affected the functional outcome. ZLP was found to be a more effective procedure in restoring grip strength, whereas FDS-4T was more effective in correcting claw hand deformity.

Adult↗

[Facial paralysis in temporal bone trauma].

OBJECTIVE: To study the cause and treatment of facial paralysis in temporal bone trauma. METHODS: A retrospective review of 28 patients with facial paralysis resulting from temporal bone trauma was conducted, House-Brackmann(H-B) system was used to evaluate the recovery of facial nerve function, U test was employed for statistic analysis. RESULTS: Twenty-six cases underwent following up facial nerve function of all patients was recovery partly after surgery, 46% cases reached H-B II, 84% cases reached H-B III, comparing facial nerve decompression within 4 months of injury to beyond 4 months of injury, recovery to H-B II or more of facial nerve function was 60% and 0%, respectively. The difference was significant(P < 0.05). CONCLUSION: Surgery decompression is effective on facial nerve palsy caused by temporal bone trauma. It is recommended that surgery decompression be carried out as soon as possible since a better prognosis is obtained if it is performed within four months after injury.

Adolescent↗

[Peripheral facial paralysis. The value of clinical neurophysiology].

AIMS: The aim of this study was to review the value of neurophysiological exploration in peripheral facial paralysis in the literature and in our own experience. METHOD: Peripheral facial paralysis is a frequently occurring cranial neuropathy with an acute presentation. Its striking clinical expression is usually in strong contrast to its benign prognosis, except for a small percentage of cases in which the existence of acute injury to the nerve (axonotmesis) will cause it to progress unfavourably, either due to the absence of nerve regeneration or because this is inadequate or insufficient. A neurophysiological study aids diagnosis and the functional and prognostic assessment. CONCLUSIONS: We recommend the utilisation of standardised studies involving a comprehensive electromyographic and electroneurographic evaluation of the facial territory, including reflexology (blink reflex). Use of a suitable methodology in the neurophysiological study of this neuropathy will allow us to complete the diagnosis and to evaluate progress, even from very early days (early surgical approach prior to the onset of nerve degeneration), all of which is decisive in the prognosis of injury throughout the process.

Blinking↗

Bilateral simultaneous facial paralysis--differential diagnosis and treatment options. A case report and review of literature.

Bilateral facial paralysis or paresis of peripheral origin is a rare condition and therefore represents a diagnostic challenge. We here present a case of a previously healthy woman who was hospitalized for symptoms of meningitis. On the second day of her hospital stay, she developed bilateral facial paresis. Later, the patient developed also tachycardia and dysrhythmias. A thorough diagnostic procedure including lumbar puncture, routine blood investigation with serological tests, MRI of the brain, Holter monitoring and transoesophageal echocardiographia, revealed meningitis with radiculitis, facial paresis and myocarditis. The clinical triad of meningitis, radiculitis and facial palsy is known as the Bannwarth Syndrome (Lyme disease). The patient was treated with ceftriaxone and recovered well. Despite repeatedly taken serological tests, Borrelia burgdorferi immunoglobulins were not detected. Acquired bilateral facial paralysis can occur in several diseases of infectious, neurological, idiopathic, iatrogenic, toxic, neoplastic or traumatic origin. In this article, we review the differential diagnoses and treatment options of bilateral facial paresis and present a scheme that is helpful in the diagnostic evaluation of this condition.

Adult↗

[Transferring neurovascular rectus femoris muscle segment for treatment of facial paralysis].

OBJECTIVE: To investigate a new technique for functional treatment of chronic facial paralysis. METHODS: Based on anatomy of intramuscular neurovascular structure in the rectus femoris muscle, 7 consecutive patients with facial paralysis were treated by using a technique of microsurgically free-transferring neurovascular rectus femoris muscle segment to the face in one-stage. Follow-ups were 10 to 24 months. RESULTS: All of the 7 patients showed significantly improvement in the appearance of the oral commissure and oral competence. No complications occurred in the donor site. CONCLUSIONS: The above mentioned technique may have the advantages of preventing the intramuscular nerve and vessel from the surgical injury during splitting the muscle. It could also maintain the transferred muscular segment in a proper tension in the recipient site.

Facial Paralysis↗

Clinical and experimental studies of large amplitude action potential of the suffered facial muscles in intratemporal facial nerve paralysis.

OBJECTIVE: To testify the phenomenon that large amplitude action potential appears at the early stage of facial paralysis, and to search for the mechanism through clinical and experimental studies. PATIENTS (ANIMALS) AND METHODS: The action potentials of the orbicular ocular and oral muscles were recorded in 34 normal persons by electromyogram instruments. The normal range of amplitude percentage was found out according to the normal distribution. One hundred patients with facial paralysis were also studied. The action potentials of facial muscles were recorded in 17 guinea pigs before and after the facial nerve was compressed and the facial nerve was examined under electromicroscope before and after the compression. RESULTS: The amplitude percentage of the suffered side to the healthy side was more than 153 percent in 6 of the 100 patients. Large amplitude action potential occured in 35 per cent guinea pigs which were performed the experiment of facial nerve compression. Electromicroscopic examination revealed separation of the lammae of the facial nerve's myelin sheath in the guinea pigs which exhibited large amplitude action potential. CONCLUSION: The facial nerve exhibited a temporary over-excitability at the early stage of facial nerve injury in some patients and guinea pigs. If the injury was limited in the myelin sheath, the prognosis was relatively good.

Action Potentials↗

Diagnosis of acute flaccid paralysis: injection injury or polio?

In many countries, the treatment of choice for all fevers is one or more injections. These injections are associated with a risk of nerve damage. If cases of poliomyelitis are not to be missed, the diagnosis of injection trauma or traumatic neuritis (TN) must be exact. The guides for distinguishing between TN and polio are not clear. It is probable that some cases of polio are misdiagnosed as TN. As three-quarters of children with paralytic polio receive injections just before the onset of paralysis, their paralysis may be mistaken for TN. Clearer guidelines are proposed, together with suggestions for better documentation of muscles injected and paralysed. All cases of reported TN should be monitored and new diagnostic guidelines published. To protect their children, mothers must be educated to understand that injections for fever can cause harm. This must be an important part of the eradication programme for poliomyelitis.

Acute Disease↗

Idiopathic facial paralysis: new therapeutic prospects with acetyl-L-carnitine.

The study population was composed of 43 patients affected by idiopathic facial paralysis (20 males and 23 females), aged between 11 and 67. The study was carried out in a double-blind, randomized, placebo controlled manner. Acetyl-L-carnitine was given in an oral dose of 3 x 1 g daily for 1 month, along with a daily oral administration of 50 mg of methylprednisolone for 14 days. The evaluation was made by means of electromyograms (EMG) of the orbicularis oculi and oris muscles, by the Schirmes lacrimation test, by stapedial reflex test and a score scale for clinical assessment of paralysis. Results so far obtained have shown an earlier functional recovery of the nerve in those patients treated with acetyl-L-carnitine. Comparison between the affected and unaffected sides of the face revealed a statistical significance in the treated group (p < 0.05) as well as the amplitudes of the muscle action potentials (MAP) between the affected sides (p < 0.01).

Acetylcarnitine↗

Type II paralysis or intermediate syndrome following organophosphorous poisoning.

Three cases of type II paralysis or intermediate syndrome following organophosphorous poisoning are reported. Two patients had an initial improvement followed by development of paralysis of neck flexors, cranial nerves, proximal muscles of the limbs and respiratory muscles, which occurred 48 to 96 hours after the poisoning. All the patients recovered completely.

Adult↗

[Diaphragm pacing for the ventilatory support of the quadriplegic patients with respiratory paralysis].

Electrical stimulation of the phrenic nerve to pace the diaphragm in patients with chronic ventilatory insufficiency has been an established therapeutic modality since William W.L. Glenn first described using radiofrequency signals in 1978 to stimulate the phrenic nerves. Before this event, patients who were ventilator-dependent and thus bedridden because of respiratory paralysis associated with quadriplegia usually anticipated little chance for physical or psychosocial rehabilitation. Two cases of C1-C2 subluxtion with cord injury and chronic ventilatory insufficiency were implanted at VGH-Taipei with diaphragm pacemaker in 1988. Postoperative phrenic nerve stimulation was given according to individual training schedule. One case with total phrenic paralysis received bilateral phrenic nerve stimulation and became weaned from the ventilator 6 months later. The other case with partially active ventilatory function received unilateral phrenic nerve stimulation to compensate the ventilation. However, its final outcome still showed the necessity of a bilateral mode to achieve adequate ventilation irrespective of strenuous training for 2 years.

Adult↗

[Paralysis of the radial nerve and supracondylar fractures of the humerus in children. A study of a series of 11 cases].

Eleven radial nerve paralyses, associated with supracondylar fractures of the humerus in children, are reported: 2 incomplete motor, 5 complete motor, 2 complete motor and partial sensory and 2 complete motor and total sensory. The palsy was noticed before any treatment in 8 cases. In the 3 other cases, the palsy was secondary to difficult and repetitive closed reduction manoeuvers. The fractures were all of the extension type, grade III in 2 cases and IV in 9 cases. The displacement of the distal fragment was posterior and medial in 8 cases. Initial treatment of the fracture was conservative in 5 cases with 2 failures and surgical in 6 cases. Nerve function recovery always followed the same sequence: extensor muscles of the wrist, then extensor muscles of the fingers and at last, extensor muscles of the thumb. Time required for full recovery varied from 4 to 6 months. Open reduction and nerve control did not seem to be better than closed reduction with regard to the required time for neurological recovery and its quality. The indications depend on the extension of the paralysis. If radial palsy is incomplete, the first therapeutic step is closed reduction, followed by surgical reduction if not possible. A primary surgical approach is proposed in cases of complete sensory and motor paralysis because of the operative findings of contusion and incarceration of the nerve which may be aggravated by blind manoeuvers.

Child↗

[Peripheral facial paralysis as the first symptom of unknown metastatic primary tumor].

The spread of metastases to the brain and the leptomeninges is usually a terminal event in patients with known malignancies. We report on two patients, in whom the diagnosis of a diffusely metastasizing carcinoma was considerably delayed by the initial symptom of a peripheral facial nerve paralysis. The clinical, neuroradiologic and cerebrospinal fluid findings are discussed. A malignant neoplasm with diffuse or focal metastasis to the leptomeninges is a rare cause of peripheral facial paralysis of unclear genesis. The necessity of a lumbar puncture plus magnetic resonance imaging of the brain to enable an early diagnosis is emphasized.

Adenocarcinoma, Mucinous↗