Brain Damage

[dqd]

[ramon]

[

It was an ex sniffer cat who along with the dog retired after CS went missing one weekend. The pic of the cat was taken when they found CS ... engaged in an unspeakable act.

Can completely understanding knowing CS and his ability to undertake unspeakable acts

[apothecary]

You're actually not damaging me at all with these baits.

Rather you're showing up the moderator's blindness (perhaps selectiveness) to your antics of deliberately trying to bait me. You're screwing yourself and making the moderator look bad.

Nah. I read every single post in this forum. It's my job.

I mod at my own discretion. I really don't care how you feel about that.

[liftyourskinnyfists]

This discussion has reinvigorated my search to try to understand my condition. The following paper I found extremely informative in trying to understand how the olfactory system works and how it may react when damaged. It can be found in full here (with pictures): http://chemse.oxfordjournals.org/cgi/conte...30/suppl_1/i133 Anything in the article appearing in bold is completely my doing.

Regeneration and Rewiring the Olfactory Bulb

Richard M. Costanzo

Department of Physiology, Virginia Commonwealth University, Richmond, VA 23298-0551, USA

Correspondence to be sent to: Richard M. Costanzo, e-mail: [email protected]

Key words: neurogenesis, odorant receptor, olfactory glomeruli, olfactory neuron, topographical mapping,

During olfactory development axons from the sensory epithelium migrate to the olfactory bulb and gradually establish connections with targeted glomeruli (Key and St John, 2002). The spatial distribution of these connections form the basis of a topographical mapping of odorant receptors onto the olfactory bulb (Vassar et al., 1994). The olfactory epithelium retains its capacity to undergo neurogenesis long after development and odorant receptors continue to establish new connections in the adult olfactory bulb. Remarkably, these newly rewired connections converge onto glomeruli in specific areas of the bulb maintaining a topographical mapping of odorant receptors. The preservation of this spatial mapping of odorant receptors onto the olfactory bulb plays an essential role in the processing of olfactory information while disruption of odorant maps results in impaired or altered olfactory function (Yee and Costanzo, 1998).

The olfactory system has become a popular model for the study of neural regeneration and the rewiring of axons following injury. Lesions to the neuroepithelium, nerve fibers and olfactory bulb all have disruptive effects on odorant receptor mapping. Regeneration and the restoration of olfactory receptor connections depend upon the degree and type of injury. For example, lesions to olfactory cells in the neuroepithelium are not reversible if the basal cell layer is destroyed. However, when spared, regeneration of the basal cells leads to a reconstitution of the sensory epithelium and a subsequent restoration of olfactory function (Iwema et al., 2004).

If thats true it seems that the my basal cell layer was not destroyed by the fall. It that we so I wouldn't be able to smell anything. During my post-injury period I've went from what they call no "olfactory function" to limited "olfactory function". This indicates to me that regeneration has been taking place and more olfactory receptor connections should keep occuring into the future.

Recovery following olfactory nerve transection also depends on the degree of injury. Extensive lesions involving damage to both the olfactory nerves and layers of the olfactory bulb are more likely to produce scar tissue and gliosis, introducing mechanical barriers to axon growth. Regenerating axons must penetrate or circumvent these obstacles if they are to successfully rewire the olfactory bulb. Early studies of olfactory nerve lesions used metal blade instruments. This often resulted in extensive damage to multiple layers of the olfactory bulb as well as the scraping of bone and dura along the cribriform plate. Very long recovery times were frequently needed to observe reconnected axons within the olfactory bulb, and connections were often formed in areas of injury extending well into the granule cell layer. Although new methods have been developed to selectively lesion the olfactory nerves with minimal or no damage to the olfactory bulb (Costanzo, 2000), regenerating nerve fibers still face the spatial challenges introduced by the disruption of axon sheath alignments at the cribriform plate. In spite of the many obstacles encountered when rewiring the olfactory bulb after injury, the olfactory system maintains its capacity to regenerate new axon processes and can reestablish functional connections with the olfactory bulb.

So my injury recovery time is dependant on the degree of injury; scare tissue and gliosis and/or damage to the olfactory bulb will all increase the time it takes to recovery.

Figure 1 illustrates the changes that occur in the rewiring of the olfactory bulbs of P2-tau-LacZ mice following nerve transection. Although regenerated axons retain their ability to converge and re-establish connections with glomeruli, these rewired connections are distributed across a very wide area of the olfactory bulb (Figure 1A) and there is significant disruption to the normal P2 odorant mapping pattern observed in control mice (Figure 1B).

View larger version (131K):

[in this window]

[in a new window]

Figure 1 Changes in P2 odorant receptor mapping after recovery from olfactory nerve transection. (A) 60 days following nerve transection regenerated P2 axons project to multiple glomeruli in different locations distributed across the olfactory bulb. ( Typical P2 mapping onto a targeted glomerulus in the olfactory bulb of a control animal.

In addition to the wider spatial distribution of P2 labeled axons projecting to multiple glomeruli, histological observations of the olfactory bulb show that many glomeruli receive partial innervation by P2 axons. These findings suggest that after nerve transection, glomeruli in the olfactory bulb are no longer dominated by a single odorant subtype and that there is a competition among regenerating receptor axons to occupy synaptic sites within a glomerulus. This post lesion alteration in the rewiring of glomeruli may have significant functional consequences, especially for odor discrimination.

If I'm understanding this correctly this is both fascinating and fills a large hole of my puzzle. One consequence of my head injury has been my inability to distinguish between odors that I would have recognized before my head trauma. Apparently the injury left a gap that was once occupied by a single type of olfactory receptor axons that recognize and discriminate certain types of odorants. These gaps were infact niches that allowed competition between a variety of olfactory receptor axons that select for various types of odorants, which would account for a mixed signal and an inability to discriminate between various odorants. Unfortunately, if thats the case then I really wouldn't fix the problem, but perhaps I could learn to reassociate different objects with their smells, similar to how a stroke victim may have to relearn certain skill such as reading or language.

I could also speculate that various neurotrophic substances if used sortly after headtrauma could avoid this mixing of receptors and retain its homologous profile after repair. Theres a lot going on here that is beyond my education but it makes sense to me that this would occur, because receptors of foreign geography, being farther away, would have to travel farther than those right next to the damage and which would likely be homologous to those that were destroyed. Again, I'm just speculating; surely one of you smart lads knows a great deal more than me about this subject and can tell me how wrong I am. The next paragraph in IMO supports this, and also leads me to believe that I injured the olfactory nerves and bulbs and not the neuroepithelium. I imagine that these receptors are so small that it would take more than an fMRI scan to "objectively" view if the axons have been accurately rewired to the olfactory bulb. I find it likely that the only indication of a problem would be through the subjective experience of the individual.

The inability of axons to accurately rewire the olfactory bulb and restore the spatial integrity of odorant receptor maps is more likely to occur following injury to the olfactory nerves and bulbs than to the neuroepithelium. When the olfactory nerves and bulbs are injured, regenerated axons must find new pathways or overcome barriers such as gliosis and the formation of scar tissue before they can reestablish connections with the bulb. In contrast, when injury is limited to the olfactory neuroepithelium, regenerating axons have access to intact nerve bundle sheaths that provide conduits to guide axons back to specific regions of the bulb.

Mechanisms that facilitate or inhibit the guidance of axons to specific targets in the olfactory bulb are topics of considerable interest. Axon–cell interactions, growth factors, the role of glia cells and axonal outgrowth and interaction with extracellular matrix molecules are all topics that need further investigation. These mechanisms are likely to play an important role in the rewiring of the olfactory bulb. Future studies directed at understanding these mechanisms may help in the development of new strategies to improve recovery and restore olfactory function following injury.

I'm gonna continue to read on this topic as the time presents itself.

Heres another good link that talks about the discovery of the olfactory receptor genes in mice: http://www.hhmi.org/senses/d120.html

Edited February 12, 2007 by liftyourskinnyfists

[mescalito]

Sounds promising,I hope you get your full range of smell back.

[coin]

http://senseofsmell.org/

http://www.scienceofsmell.com/