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Accessory Bulb:
[edit]The vomernasal organ (VMO) sends projections to the accessory olfactory bulb which forms the vomernasal (accessory) olfactory system. [1] In order for the vomernasal pump to turn on the main olfactory epithelium must first detect the appropriate odor. [2] The vomernasal organ then send axonal projections to the accessory olfactory bulb. The accessory olfactory bulb provides direct excitatory inputs to the principle neurons called mitral cells [3] which are transmitted to the amygdala and the hypothalamus, directly involved in sex hormone activity. [4] Axons of the vomeronasal sensory neurons express a given receptor type which diverge between 6 and 30 glomeruli in the accessory olfactory bulb. Mitral cell dendritic endings go through a dramatic period of targeting and clustering just after presynaptic unification of the sensory neuron axons. The vomernasal sensory neurons to mi- tral cell connectivity is precise, with mitral cell dendrites targeting glomeruli.[3]
The area of the brain related to olfactory processing is much larger in rodents than in humans. This means that animal olfactory systems for example rodents are much stronger than those of humans. The accessory olfactory bulb is good at detecting single pheromones or pheromonal blends within a complex chemical background such as body odor because the vomernasal receptor neurons are narrowly tuned. This system is important for animals because the detection of pheromones helps in the mating process as well as the recognition of individuality. Although the accessory olfactory bulb participates in individual descrimination its' chemosignal detection is unknown.[5]
Olfactory Dysfunctions
[edit]Olfactory problems can be divided into different types based on their malfunction. The olfactory dysfunction can be total called anosmia, incomplete like partial anosmia, hyposmia, or microsmia, distorted such as dysosmias, and spontaneous sensations like phantosmias. The inability to recognize odors can occur independently of a normally function olfactory system called olfactory agnosia. The rare condition of abnormally acute smell function is called hyperosmia. Like vision and hearing, the olfactory problems can be bilateral or unilateral meaning if a person has anosmia on the right side of the nose but not the left, it is a unilateral right anosmia. On the other hand, if it is on both sides of the nose it is called bilateral anosmia or total anosmia. [6]
Causes of Olfactory Dysfunction
[edit]There are 5 more common causes of olfactory dysfunction: Viral Infections, Age, Exposure to Toxic Chemicals, Head Truama, and Neurodegenerative diseases.[6]
Viral Infections
[edit]The most common cause of permanent hyposmia and anosmia is upper respiratory infections. Such dysfunctions, show no change over time and can sometimes reflect damage not only in the olfactory epithelium but also to the central olfactory structures as a resutl of viral invasions into the brain. Among these virus-realted disorder are the common cold, hepatitis, flu-lie infections, and herpes. Most viral infections are unrecognizable because they are so mild or entirely asymptomatic.[6]
Age
[edit]Age is the primary cause of olfactory decline in healthy adults having more impact than cigarette smoking. Age-related changes in smell function often go unnoticed and small ability is rarely tested clinically unlike hearing and vision. 2% of people under 65 years of age have chronic smelling problems. This increases greatly between people of ages 65 and 80 with about half experiencing significant problems smelling. Then for adults over 80, the numbers rise to almost 75%. [7] The basis for age-related changes in smell function include closure of the cribriform plate,[6] and cumulative damage to the olfactory receptors from repeated viral and other insults throughout life.
Exposure to Toxic Chemicals
[edit]Chronic exposure to some airborne toxins such as heribicides, pesticides, solents, and heavy metals (cadmium, chromium, nickel, and manganese), can alter the ability to smell.[8] These agents not only damage the olfactory epithelium but they are likely to enter the brain via the olfactory mucosa.[9]
Head Trauma
[edit]Trauma-related olfactory dysfunction depends on the severity of the trauma and whether strong acceleration/deceleration of the head occurred. Occipital and side impact causes more damage to the olfactory system than frontal impact. [10]
Neurodegenerative Diseases
[edit]Neurologists have observed that olfactory dysfunction is a cardinal feature of several neurodegenerative diseases such as Alzheimer's Disease and Parkinson's Disease. Most of these patients are unaware of an olfactory deficit until after testing where 85% to 90% of early-stage patients showed decrease activity in central odor processing structures. [11]
Other neurodegenerative diseases that affect olfactory dysfunction include Huntington's disease, multiinfract dementia, amyotrophic lateral sclerosis, and schizophrenia. These diseases more moderately affect the smelling system than Alzheimer's disease and Parkinson's disease.[12] Furthermore, progressive supranculear palsy and parkinsonism are associated with only minor olfactory problems. These findings have led to the suggestion that olfactory testing may help in the diagnosis of several different neurodegenerative diseases.[13]
Neurodegenerative diseases with well-established genetic determinants are also associated with olfactory dysfunction. Such dysfunction, for example, is found in patients with familial Parkinson's disease and those with Down syndrome.[14] But further studies have concludedd that olfactory loss may be associated with retardation, rather than Alzheimer's disease like pathology.[15]
Huntington's disease is also associated with problems in odor identification, detection, discrimination, and memory. The problem is prevalent once the phenotypic elements of the disorder appear, although it is unknown how far in advance the olfactory loss precedes the phenotypic expression.[6]
References
[edit]- ^ Taniguchi, K.; Saito, S.; Taniguchi, K. (2011 Feb). "Phylogenic outline of the olfactory system in vertebrates". The Journal of Veterinary Medical Science / The Japanese Society of Veterinary Science. 73 (2): 139–47. doi:10.1292/jvms.10-0316. PMID 20877153.
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(help) - ^ Slotnick, Burton; Restrepo, Diego; Schellinck, Heather; Archbold, Georgina; Price, Stephen; Lin, Weihong (2010). "Accessory olfactory bulb function is modulated by input from the main olfactory epithelium". European Journal of Neuroscience. 31 (6): 1108–1116. doi:10.1111/j.1460-9568.2010.07141.x. PMC 3745274. PMID 20377623.
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ignored (help)CS1 maint: date and year (link) - ^ a b Hovis, Kenneth R. (6). "Activity Regulates Functional Connectivity from the Vomeronasal Organ to the Accessory Olfactory Bulb" (PDF). The Journal of Neuroscience. 32 (23): 7907–7916. doi:10.1523/JNEUROSCI.2399-11.2012. PMC 3483887. PMID 22674266. Retrieved 10 November 2013.
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mismatch (help); Unknown parameter|coauthors=
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suggested) (help); Unknown parameter|month=
ignored (help) - ^ Trotier, D (September 2011). "Vomeronasal organ and human pheromones". European Annals of Otorhinolaryngology, Head and Neck Diseases. 128 (4): 184–190. doi:10.1016/j.anorl.2010.11.008. PMID 21377439. Retrieved 10 November 2013.
{{cite journal}}
: CS1 maint: date and year (link) - ^ Restrepo, Diego; Arellano, Julie; Oliva, Anthony M.; Schaefer, Michele L.; Lin, Weihong (2004). "Emerging views on the distinct but related roles of the main and accessory olfactory systems in responsiveness to chemosensory signals in mice". Hormones and Behavior. 46 (3): 247–256. doi:10.1016/j.yhbeh.2004.02.009. PMID 15325226. S2CID 10842265. Retrieved 10 November 2013.
- ^ a b c d e Doty, Richard (12 February 2009). "The Olfactory System and Its Disorders". Seminars in Neurology. 29 (1): 074–081. doi:10.1055/s-0028-1124025. PMID 19214935. S2CID 260319226.
- ^ Doty, Richard L.; Shaman, Paul; Dann, Michael (1984). "Development of the university of pennsylvania smell identification test: A standardized microencapsulated test of olfactory function". Physiology & Behavior. 32 (3): 489–502. doi:10.1016/0031-9384(84)90269-5. PMID 6463130. S2CID 30923277.
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ignored (help)CS1 maint: date and year (link) - ^ Doty, RL (2001). "Neurotoxic exposure and olfactory impairment". Clin Occupat Environ Med. 1: 547–575.
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suggested) (help) - ^ Tjalve, H (1996; 79(6): 347-356). "Uptake of manganese and cadmium from the nasal mucosa into the central nervous system via olfactory pathways in rats". Pharmacol Toxicol. 79 (6): 347–356. doi:10.1111/j.1600-0773.1996.tb00021.x. PMID 9000264.
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suggested) (help)CS1 maint: year (link) - ^ Doty, RL (1997). "Olfactory dysfunction in patients with head trauma". Arch Neurol. 54 (9): 1131–1140. doi:10.1001/archneur.1997.00550210061014. PMID 9311357.
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suggested) (help) - ^ Quinn, N. P.; Rossor, M. N.; Marsden, C. D. (1 January 1987). "Olfactory threshold in Parkinson's disease". Journal of Neurology, Neurosurgery & Psychiatry. 50 (1): 88–89. doi:10.1136/jnnp.50.1.88. PMID 3819760. S2CID 42326842.
- ^ Doty, Richard L.; Bromley, Steven M.; Stern, Matthew B. (1995). "Olfactory Testing as an Aid in the Diagnosis of Parkinson's Disease: Development of Optimal Discrimination Criteria". Neurodegeneration. 4 (1): 93–97. doi:10.1006/neur.1995.0011. PMID 7600189.
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ignored (help)CS1 maint: date and year (link) - ^ Doty, R. L.; Golbe, L. I.; McKeown, D. A.; Stern, M. B.; Lehrach, C. M.; Crawford, D. (1 May 1993). "Olfactory testing differentiates between progressive supranuclear palsy and idiopathic Parkinson's disease". Neurology. 43 (5): 962. doi:10.1212/WNL.43.5.962. PMID 8492953. S2CID 41865918.
- ^ Chen, Margaret A.; Lander, Timothy R.; Murphy, Claire (2006). "Nasal health in Down syndrome: A cross-sectional study". Otolaryngology - Head and Neck Surgery. 134 (5): 741–745. doi:10.1016/j.otohns.2005.12.035. PMID 16647527. S2CID 21198608.
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ignored (help)CS1 maint: date and year (link) - ^ McKeown, D. A.; Doty, R. L.; Perl, D. P.; Frye, R. E.; Simms, I.; Mester, A. (1 October 1996). "Olfactory function in young adolescents with Down's syndrome". Journal of Neurology, Neurosurgery & Psychiatry. 61 (4): 412–414. doi:10.1136/jnnp.61.4.412. PMC 486586. PMID 8890783.