Electrical stimulation as a therapeutic option to improve eyelid function in chronic facial nerve disorders.
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)
Spontaneous CSF otorrhea caused by abnormal development of the facial nerve canal.
In two patients with surgically proved CSF fistula through the facial nerve canal, MR and CT examinations showed smooth enlargement of the geniculate fossa with CSF signal. In the clinical setting of CSF otorrhea or rhinorrhea, the presence of an enlarged labyrinthine facial nerve canal and enlarged geniculate fossa on CT scans and CSF intensity on MR images strongly suggests a CSF fistula through the facial nerve canal. (+info)
Ramsay Hunt syndrome associated with brain stem enhancement.
Postcontrast T1-weighted MR images in a patient with Ramsay Hunt syndrome showed an enhancing lesion in the region of the nucleus of the pontine facial nerve and abnormal enhancement of the intrameatal, labyrinthine, and tympanic facial nerve segments and of the geniculate ganglion, as well as enhancement of the vestibulocochlear nerve and parts of the membranous labyrinth. This enhancement most probably resulted from a primary neuritis of the intrameatal nerve trunks of the seventh and eighth cranial nerves. (+info)
Cardiac inotropic, chronotropic, and dromotropic actions of subretrofacial neurons of cat RVLM.
The cardiac actions of microinjecting sodium glutamate (0.5-2 nmol) among sympathetic premotor neurons of the subretrofacial nucleus in the rostral ventrolateral medulla (RVLM) were studied in chloralose-anesthetized cats after bilateral vagotomy, sinoaortic denervation, adrenalectomy, and alpha1-receptor blockade. Glutamate microinjections increased heart rate by 25.9 +/- 1.8 beats/min (17. 5%), systolic rate of rise in left ventricular pressure (LVdP/dt) by 1,443 +/- 110 mmHg/s (119%), and arterial blood pressure by 26.9 +/- 1.7 mmHg (50%), whereas they shortened the electrocardiogram P-R interval in 85 of 103 cases by 7.5 +/- 1.2 ms (11.4%), triggering junctional rhythms on five occasions. The increase in LVdP/dt usually led the rise in blood pressure, and its magnitude greatly exceeded any increase attributable to changes in heart rate, diastolic filling, or afterload. Right-sided microinjections caused significantly greater tachycardias than did left-sided microinjections, but only left-sided microinjections triggered junctional rhythms (5 of 52 vs. 0 of 51; P < 0.05), whereas microinjections on either side raised LVdP/dt equally. Subretrofacial neurons thus drive positive chronotropic, inotropic, and dromotropic actions via the cardiac sympathetic nerves, whereas subsets among them preferentially control different aspects of cardiac function. (+info)
Isolated dysarthria due to extracerebellar lacunar stroke: a central monoparesis of the tongue.
OBJECTIVES: The pathophysiology of dysarthria can preferentially be studied in patients with the rare lacunar stroke syndrome of "isolated dysarthria". METHODS: A single study was carried out on seven consecutive patients with sudden onset of isolated dysarthria due to single ischaemic lesion. The localisation of the lesion was identified using MRI. The corticolingual, cortico-orofacial, and corticospinal tract functions were investigated using transcranial magnetic stimulation. Corticopontocerebellar tract function was assessed using 99mTc hexamethylpropylene amine oxime-single photon emission computerised tomography (HMPAO-SPECT) in six patients. Sensory functions were evaluated clinically and by somatosensory evoked potentials. RESULTS: Brain MRI showed the lesions to be located in the corona radiata (n=4) and the internal capsule (n=2). No morphological lesion was identified in one patient. Corticolingual tract function was impaired in all patients. In four patients with additional cortico-orofacial tract dysfunction, dysarthria did not differ from that in patients with isolated corticolingual tract dysfunction. Corticospinal tract functions were normal in all patients. HMPAO-SPECT showed no cerebellar diaschisis, suggesting unimpaired corticopontocerebellar tract function. Sensory functions were not affected. CONCLUSION: Interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of isolated dysarthria after extracerebellar lacunar stroke. (+info)
MR imaging of Dejerine-Sottas disease.
We report the MR findings in two patients with clinically and histologically proved Dejerine-Sottas disease. One patient had spinal involvement with multiple thickened and clumped nerve roots of the cauda equina; the second had multiple enlarged and enhancing cranial nerves. Although these findings are not specific for Dejerine-Sottas disease, they are suggestive of the diagnosis, which is further corroborated with history and confirmed with sural nerve biopsy and laboratory studies. (+info)
Hoxa2 and Hoxb2 control dorsoventral patterns of neuronal development in the rostral hindbrain.
Little is known about how the generation of specific neuronal types at stereotypic positions within the hindbrain is linked to Hox gene-mediated patterning. Here, we show that during neurogenesis, Hox paralog group 2 genes control both anteroposterior (A-P) and dorsoventral (D-V) patterning. Hoxa2 and Hoxb2 differentially regulate, in a rhombomere-specific manner, the expression of several genes in broad D-V-restricted domains or narrower longitudinal columns of neuronal progenitors, immature neurons, and differentiating neuronal subtypes. Moreover, Hoxa2 and Hoxb2 can functionally synergize in controlling the development of ventral neuronal subtypes in rhombomere 3 (r3). Thus, in addition to their roles in A-P patterning, Hoxa2 and Hoxb2 have distinct and restricted functions along the D-V axis during neurogenesis, providing insights into how neuronal fates are assigned at stereotypic positions within the hindbrain. (+info)
Exacerbation of facial motoneuron loss after facial nerve transection in severe combined immunodeficient (scid) mice.
The immune system functions to protect an organism against microbial infections and may be involved in the reparative response to nerve injury. The goal of this study was to determine whether the immune system plays a role in regulating motoneuron survival after a peripheral nerve injury. After a right facial nerve axotomy, facial motoneuron (FMN) survival in C.B-17 (+/+) wild-type mice was found to be 87 +/- 3.0% of the unaxotomized left side control. In contrast, facial nerve axotomy in C.B-17 (-/-) severe combined immunodeficient (scid) mice, lacking functional T and B lymphocytes, resulted in an average FMN survival of 55 +/- 3.5% relative to the unaxotomized left side control. This represented an approximately 40% decrease in FMN survival compared with wild-type controls. The reconstitution of scid mice with wild-type splenocytes containing T and B lymphocytes restored FMN survival in these mice to the level of the wild-type controls. These results suggest that immune cells associated with acquired immunity play a role in regulating motoneuron survival after a peripheral nerve injury. (+info)