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Results for “GENICULATE GANGLION”

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At least 55 records · Page 3Linked to original sources
PubMed1994

Polymerase chain reaction amplification of herpes simplex viral DNA from the geniculate ganglion of a patient with Bell's palsy.

Bell's palsy is the most common cause of facial paralysis. In this study, we demonstrate the presence of herpes simplex viral type 1 (HSV-1) genomic DNA in the geniculate ganglion of a patient who had Bell's palsy. This association suggests that in this patient, HSV-1 may have caused Bell's palsy. If HSV-1 is a cause of Bell's palsy, treatment with acyclovir may be beneficial. Additional studies should be done to establish the prevalence of HSV-1 as an etiologic agent of Bell's palsy.

Aged↗
PubMed1997

Geniculate ganglion meningioma.

Primary ectopic meningiomas are rare, but may be seen in the head and neck region. The temporal bone and its neural foramen are rarely the site of a primary meningioma. This report describes the CT and MRI appearance of an ectopic meningioma arising at the anatomic location of the geniculate ganglion, and discusses the differential diagnosis as well as the possible origin of the tumor.

Adolescent↗
PubMed2005

Temperature modulates taste responsiveness and stimulates gustatory neurons in the rat geniculate ganglion.

In humans, temperature influences taste intensity and quality perception, and thermal stimulation itself may elicit taste sensations. However, peripheral coding mechanisms of taste have generally been examined independently of the influence of temperature. In anesthetized rats, we characterized the single-cell responses of geniculate ganglion neurons to 0.5 M sucrose, 0.1 M NaCl, 0.01 M citric acid, and 0.02 M quinine hydrochloride at a steady, baseline temperature (adapted) of 10, 25, and 40 degrees C; gradual cooling and warming (1 degrees C/s change in water temperature >5 s) from an adapted tongue temperature of 25 degrees C; gradual cooling from an adapted temperature of 40 degrees C; and gradual warming from an adapted temperature of 10 degrees C. Hierarchical cluster analysis of the taste responses at 25 degrees C divided 50 neurons into two major categories of narrowly tuned (Sucrose-specialists, NaCl-specialists) and broadly tuned (NaCl-generalists(I), NaCl- generalists(II), Acid-generalists, and QHCl-generalists) groups. NaCl specialists were excited by cooling from 25 to 10 degrees C and inhibited by warming from 10 to 25 degrees C. Acid-generalists were excited by cooling from 40 to 25 degrees C but not from 25 to 10 degrees C. In general, the taste responses of broadly tuned neurons decreased systematically to all stimuli with decreasing adapted temperatures. The response selectivity of Sucrose-specialists for sucrose and NaCl-specialists for NaCl was unaffected by adapted temperature. However, Sucrose-specialists were unresponsive to sucrose at 10 degrees C, whereas NaCl-specialists responded equally to NaCl at all adapted temperatures. In conclusion, we have shown that temperature modulates taste responsiveness and is itself a stimulus for activation in specific types of peripheral gustatory neurons.

Action Potentials↗
PubMed1996

[Cavernous hemangioma of the geniculate ganglion. Value of otoneurosurgical collaboration].

A patient with a progressive peripheral facial paralyses should be considered to have a tumor involved the facial nerve until proved otherwise. Haemangiomas of the temporal bone are uncommon and the present study discusses pathology, clinical presentation and therapeutic management of a tumor located at the geniculate ganglion. Complete surgical removal by the middle fossa approach is the treatment of choice with adequate margins and preservation of adjacent structures when it is oncologically possible. The surgeon must be familiar with all aspects of facial nerve repair.

Adult↗
PubMed2002

Chickenpox and the geniculate ganglion: facial nerve palsy, Ramsay Hunt syndrome and acyclovir treatment.

Facial nerve palsy has long been considered to have an infectious etiology. Recent diagnostic analyses in children and adults have provided convincing evidence that reactivation of varicella-zoster virus (VZV), sometimes during infectious mononucleosis, can lead to cranial nerve VII palsy. The site of reactivation from latency is the geniculate ganglion. Virus most likely enters the ganglion during chickenpox, via the sensory branches of the facial nerve located on the ear and tongue. Retrospective reviews suggest that patients with VZV-related facial nerve palsy have poorer outcomes than other cases of Bell's palsy. Therefore treatment with acyclovir is suggested when VZV reactivation i slikely.

Adult↗
PubMed1992

Presence of gastrin-releasing peptide in neurons of the geniculate ganglion in rat and man.

Gastrin-releasing peptide (GRP) was demonstrated by immunohistochemistry and high-performance liquid chromatography to be present in the great majority of neurons in the geniculate ganglion of rat and man. This was in contrast to findings in the sphenopalatine ganglion of rat, where only little GRP was found, and in the otic, trigeminal, glossopharyngeal-vagal and internal carotid ganglia, where no GRP-containing cells could be demonstrated. The peptide was not detected by immunohistochemistry in nerve fibers within structures innervated from the ganglion (tongue, soft palate, retroauricular skin and facial musculature). The retrograde axonal tracer True blue accumulated in these neurons of rat after application not only in the tongue and soft palate but also in the retroauricular skin.

Animals↗
PubMed2004

Developmental expression of neurotrophin receptor genes in rat geniculate ganglion neurons.

Individual neurons dissected from immunohistochemically stained paraffin sections of the developing rat geniculate (VIIth cranial) ganglion were assayed for their content of mRNA of the neurotrophin receptor genes, p75 , trkA , trkB and trkC. Fetal and postnatal rats, from the 13th embryonic day (E13) until the 20th postnatal day (P20), were used. Single cells were subjected to RNA amplification, followed by treatment with reverse transcriptase and DNA amplification by the polymerase chain reaction (PCR). The identity of the PCR products was verified by subcloning and sequencing. A total of 227 neurons were examined, of which 212 (93%) gave a PCR signal for at least one neurotrophin receptor. We found: (1) Approximately half of the neurons expressed more than one receptor. (2) A truncated version of trkB , possessing the ligand-binding region but lacking the tyrosine kinase domain, occurred quite frequently, often in combination with the full-length trkB, with trkA or both. (3) The pattern of staining for trkB-like immunoreactivity was usually predictive that either its full length or truncated mRNA would be present. This was not the case for trkC-like immunoreactivity. Western blots on E15 brain tissue showed no band for full-length trkC ( approximately 150 kDa), suggesting the antibody may have been immunoreactive with a truncated ( approximately 120 kDa) but not a full-length version of the trkC receptor. (4) The pattern of neurotrophin receptor gene expression changed during development. (5) p75 expression occurred infrequently--in only 7 of the 212 neurons that gave a signal for any receptor.

Animals↗