Facial diplegia complicating a bilateral internal carotid artery dissection. (1/297)

BACKGROUND AND PURPOSE: We report a case of facial diplegia complicating a bilateral internal carotid artery dissection. CASE DESCRIPTION: A 49-year-old patient presented with unilateral headache and oculosympathetic paresis. Cerebral angiography revealed a bilateral internal carotid artery dissection. A few days later, the patient developed a facial diplegia that regressed after arterial recanalization. An arterial anatomic variation may explain this ischemic complication of carotid dissection. CONCLUSIONS: Double carotid dissection should be included among the causes of bilateral seventh nerve palsy.  (+info)

Electrical stimulation as a therapeutic option to improve eyelid function in chronic facial nerve disorders. (2/297)

PURPOSE: To establish whether it is possible to improve orbicularis oculi muscle function in the eyelids of patients with a chronic seventh cranial nerve palsy by using transcutaneous electrical stimulation to the point at which electrical stimulation induces a functional blink. METHODS: Ten subjects (one woman, nine men) aged 36 to 76 with chronic, moderate to severe facial nerve palsy were recruited into the study. Voluntary and spontaneous eyelid movements were assessed, using an optical measuring system, before, during, and after a 3-month treatment period. Voluntary and spontaneous lid velocities were also measured and compared with eyelid kinematic data in normal subjects (12 women, 18 men; age range, 22-56 years). RESULTS: Therapeutic electrical stimulation applied over 3 months produced improvement in eyelid movement (>2 mm) in 8 of 10 patients during voluntary eyelid closure. However, there was no significant improvement recorded in spontaneous blink amplitudes or peak downward-phase velocity of the upper eyelid. This regimen of stimulation failed to recover function well enough that a functional blink could be induced in the paretic eyelid by electrical stimulation. CONCLUSIONS: Electrical stimulation using transcutaneous electrical nerve stimulators units can improve voluntary eye closure, apparently because of a reduction in stiffness of eyelid mechanics, rather than an improvement of muscle function. Investigation of alternative stimulation regimens is warranted.  (+info)

Clinical characteristics of CHARGE syndrome. (3/297)

CHARGE syndrome, first described by Pagon, was named for its six major clinical features. They are: coloboma of the eye, heart defects, atresia of the choanae, retarded growth and development including CNS anomalies, genital hypoplasia and/or urinary tract anomalies, and ear anomalies and/or hearing loss. We experienced three cases of CHARGE syndrome who displayed ocular coloboma, heart defects, retarded growth and development, and external ear anomalies, and we also review the previously reported literature concerning CHARGE syndrome.  (+info)

Successful oral doxycycline treatment of Lyme disease-associated facial palsy and meningitis. (4/297)

Twenty-nine patients, aged 11-79 years (mean, 50 years), with Lyme neuroborreliosis, facial nerve palsy, and meningitis were treated with oral doxycycline (daily dose, 200-400 mg) for 9-17 days in a prospective, nonrandomized study. Facial paresis was bilateral in eight (28%) of the 29 patients. Twenty-six patients (90%) recovered without sequelae within 6 months, while three of the patients with bilateral facial palsy at admission had remaining paresis at follow-up. In five patients, contralateral facial paresis developed 1-12 days after initiation of therapy, and two patients were retreated with antibiotics. Posttreatment examinations of cerebrospinal fluid showed a marked decrease of inflammatory cells and protein concentrations compared with pretreatment levels in all followed up patients. The favorable clinical outcome agrees with findings of other reports on intravenous antibiotic therapy for Lyme disease-associated meningitis with facial palsy. Our conclusion is that oral doxycycline is an effective and convenient therapy for Lyme disease-associated facial palsy.  (+info)

Physical therapy for facial paralysis: a tailored treatment approach. (5/297)

BACKGROUND AND PURPOSE: Bell palsy is an acute facial paralysis of unknown etiology. Although recovery from Bell palsy is expected without intervention, clinical experience suggests that recovery is often incomplete. This case report describes a classification system used to guide treatment and to monitor recovery of an individual with facial paralysis. CASE DESCRIPTION: The patient was a 71-year-old woman with complete left facial paralysis secondary to Bell palsy. Signs and symptoms were assessed using a standardized measure of facial impairment (Facial Grading System [FGS]) and questions regarding functional limitations. A treatment-based category was assigned based on signs and symptoms. Rehabilitation involved muscle re-education exercises tailored to the treatment-based category. OUTCOMES: In 14 physical therapy sessions over 13 months, the patient had improved facial impairments (initial FGS score= 17/100, final FGS score= 68/100) and no reported functional limitations. DISCUSSION: Recovery from Bell palsy can be a complicated and lengthy process. The use of a classification system may help simplify the rehabilitation process.  (+info)

Autosomal dominant optic atrophy with unilateral facial palsy: a new hereditary condition? (6/297)

A mother and daughter are reported with bilateral optic atrophy with onset in infancy and unilateral facial palsy. This appears to be a novel autosomal dominant disorder.  (+info)

The puzzle of autism: an ophthalmologic contribution. (7/297)

PURPOSE: A previous study of 86 thalidomide-affected subjects with ophthalmic manifestations revealed the unexpected finding of autism in 4 of the 5 severely retarded individuals. The subjects had anomalies associated with an early gestational effect of thalidomide, including facial nerve palsy and incomitant strabismus. Because autism has been observed in a few cases of Mobius sequence (Mobius syndrome), a condition characterized by involvement of the sixth and seventh cranial nerves, the similarity to early thalidomide embryopathy suggested a relation between cranial nerve involvement and autism. The present study was undertaken to further evaluate the association of autism with patients manifesting findings of Mobius syndrome. METHODS: A prospective study of 25 Swedish patients with Mobius sequence was conducted. The patients had a complete multidisciplinary evaluation, including ophthalmologic and psychiatric examinations and standard testing for autism. Findings associated with autism were compared with the ocular and systemic anomalies of the 4 thalidomide-affected subjects. RESULTS: In the Mobius group 6 patients had autism, achieving the criteria for autism according to all the diagnostic manuals that were used. One patient showed autistic-like conditions meeting fewer numbers of the criteria. A few were too young to be meeting evaluated. Incomitant strabismus ranging from primary abduction defects alone to a horizontal gaze paresis pattern was noted in these patients, in addition to characteristic findings of seventh nerve paresis. Aberrant lacrimation was observed in many cases, especially often associated with autism. CONCLUSION: The common group of anomalies noted in both cases of thalidomide embryopathy and Mobius sequence suggests that brain-stem damage probably early in embryogenesis can sometimes be associated with autism.  (+info)

Genetic factors in human sleep disorders with special reference to Norrie disease, Prader-Willi syndrome and Moebius syndrome. (8/297)

Sleep-wake problems are common in specific inborn errors of metabolism and structure of the central nervous system. Psychological factors, behavioural difficulties, metabolic disturbances, and widespread rather than focal damage to the nervous system are present in many of these diseases and all influence the sleep-wake cycle. However, a number of conditions cause relatively focal damage to the neuroanatomical substrate of sleeping and waking. These include fatal familial insomnia, with involvement of the prion protein gene on chromosome 20, Norrie disease, the Prader-Willi syndrome and the Moebius syndrome. The last three important conditions, although rare, are considered in detail in this review. They result in sensory deprivation, hypothalamic and mid-brain damage, and involve the X-chromosome, chromosome 15, and chromosome 13, respectively. These conditions cause a wide variety of sleep disturbance, including parasomnias, daytime sleepiness, and a condition like cataplexy. The place of the relevant gene products in normal sleep regulation needs further exploration.  (+info)