Disease relevance of Cranial Nerves

• Together, these data suggest a pathogenic role of MBP-specific T cells in inflammatory demyelination within the brainstem and cranial nerve roots during the progression of MS [1].
• Npn-2 is required for the organization and fasciculation of several cranial nerves and spinal nerves [2].
• The clinical and radiographic stigmata of sclerosteosis permit differentiation from the other disorders of the "osteopetrosis" or "Albers-Schönberg disease" group, in which bony thickening and cranial nerve palsy occur [3].
• Neurofibromatosis 2 (NF2) is an autosomal dominant disease that is characterized by tumors on the vestibular branch of the VIII cranial nerve, but other types of nervous system tumors usually occur as well [4].
• The pathophysiology of reflexes mediated by the fifth and seventh cranial nerves has been studied in 16 patients with blepharospasm and oromandibular dystonia compared with normal age-matched subjects [5].

High impact information on Cranial Nerves

• LHRH-expressing neurons are also found in the nervus terminalis, a cranial nerve that is a part of the accessory olfactory system and which projects directly from the nose to the septal-preoptic nuclei in the brain [6].
• Hybridization histochemistry reveals a similar distribution of alpha- and beta-CGRP mRNA's, but their relative levels of expression vary in different cranial nerve nuclei [7].
• Taken together, these results suggest that the molecular program governing the development and maintenance of the VIIth cranial nerve is dependent upon Hoxb1, both in the neural crest-derived glia and in the facial branchiomotor neurons [8].
• In addition, radioligand binding at multiple sites of transient expression of AII receptors in 2-week-old rats, including several thalamic nuclei, the nuclei of the 3rd and 12th cranial nerves, geniculate bodies, cerebellum, and cingulate cortex, was displaced by the AT2 antagonists but not by DuP 753 [9].
• Loss of the Sall3 gene leads to palate deficiency, abnormalities in cranial nerves, and perinatal lethality [10].

Chemical compound and disease context of Cranial Nerves

• Steroid therapy was associated with improvement of the cranial nerve palsies [11].
• Toxicity included mild to moderate nausea and vomiting, transient, reversible myelosuppression, transient elevations of serum blood urea nitrogen (BUN) and creatinine and liver enzymes, infections, and self-limiting neurotoxicity characterized by changes in mental status, motor dysfunction, cranial nerve palsy, cerebellar dysfunction, and seizures [12].
• Arterial encasement and cranial nerve displacement in a case of cholesterol granuloma of the petrous apex [13].
• An intermediate syndrome characterized by respiratory paresis, weakness in the territory of several motor cranial nerves and of proximal limb and neck flexor muscles, persisted for 3 weeks [14].
• Encephalopathy and cranial nerve palsies caused by intentional trichloroethylene inhalation [15].

Biological context of Cranial Nerves

• Binding sites in these cranial nerve nuclei and tongue muscles were of high affinity, limited capacity, with steroid specificity; and they were capable of translocation to the cell nuclei in vivo [16].
• In experimental methylmercury poisoning, cranial nerve V and sensory dorsal root ganglia, which lie in regions of vascular permeability, are particularly susceptible [17].
• These results are consistent with the idea that sex differences in AR could account for sex differences observed in nerve regeneration and neuron loss following cranial nerve injury [18].
• These results indicate that intrinsic sex differences in AR levels and androgenic regulation of AR exist in cranial nerve motor nuclei, and that there are differences in the abundance and distribution pattern of AR responsive neurons in cranial nerve motor nuclei [18].
• Sclerosteosis is a rare, potentially lethal skeletal disorder in which massive bony over-growth leads to facial distortion, cranial nerve compression and progressive rise in intracranial pressure [19].

Anatomical context of Cranial Nerves

• Tbx1 mutation causes multiple cardiovascular defects and disrupts neural crest and cranial nerve migratory pathways [20].
• Within ganglia of the Vth, IXth and Xth cranial nerves, levels of NGF-R mRNA were higher in regions containing placode-derived neurons, than in regions with neural-crest-derived neurons [21].
• Like mouse Hoxb1, zebrafish hoxb1a is required for migration of the VIIth cranial nerve branchiomotor neurons from their point of origin in hindbrain rhombomere 4 towards the posterior [22].
• Hoxa1 and Hoxb1 synergize in patterning the hindbrain, cranial nerves and second pharyngeal arch [23].
• Targeted deletion of the Phox2a gene affects part of the structures in which it is expressed: the locus coeruleus, visceral sensory and parasympathetic ganglia and, as we show here, the nuclei of the IIIrd and IVth cranial nerves [24].

Associations of Cranial Nerves with chemical compounds

• MRI with gadolinium demonstrated enhancement of cranial nerve VIII bilaterally [25].
• Cranial nerve deficit: a clue to the diagnosis of ethylene glycol poisoning [26].
• This is suggested by the male-to-female ratio of the disease, the age of onset, and the sparing of neurons of cranial nerves III, IV, and VI that coincidentally lack androgen receptors [27].
• 5. By applying the nicotine through a single Perspex ring which could be moved stepwise along and across the medulla, the nicotine sensitive area was localized and the highest sensitivity was found in a region around and a little caudal to the rootlets of the XIIth cranial nerve [28].
• The syndrome occurred also in a nonobese patient receiving parenteral hyperalimentation and involved cranial nerves [29].

Gene context of Cranial Nerves

• Furthermore, fusions of cranial nerves IX and X and defects in cranial nerve V were apparent in some Lmo4(-/-) and Lmo4(+/-) mice [30].
• However, using an RNA rescue approach, we reveal that these duplicated genes do not have interchangeable biochemical functions: only hoxb1a can properly pattern the VIIth cranial nerve [22].
• This finding further supports the role of EGR2 in cranial nerve development [31].
• DM20 is expressed in the CNS only, while MBP transcripts are detected both in the CNS and in Schwann cells of the lateral line, cranial nerves, and spinal motor nerves [32].
• No specific immunoreactivity for BDNF or NT-3 was detected on the day of birth (P0) in any auditory structure, although fibers comprising the spinal tract of the Vth cranial nerve were well labelled with antibodies against BDNF [33].

Analytical, diagnostic and therapeutic context of Cranial Nerves

• Nasopharyngeal carcinoma with cranial nerve palsy: the importance of MRI for radiotherapy [34].
• The perikarya of three genera, Pleurodeles, Xenopus, and Discoglossus, were located in the brainstem by applying retrograde tracers to the appropriate cranial nerves and choline acetyltransferase immunohistochemistry was used to identify cholinergic neurons [35].
• The activity of 48 respiratory units in the paraolivary region from the middle to the rostral end of the hypoglossal cranial nerve root, and the effect of electrical stimulation and L-glutamate applied to the region on phrenic nerve activity was investigated in 14 rabbits [36].
• Neurological examination revealed several cranial nerve abnormalities and hyperreflexia, raising the suspicion of a cervicomedullary junction lesion [37].
• After careful dissection of the cranial nerves projecting to the orbit, different segments of each cranial nerve were processed for immunohistochemical analysis for TH [38].

References