Since you all are starting to throw around studies, here's a set of 43 
articles/etc.,  that I pulled from scholar.google.com.
http://tinyurl.com/2gd9z3

Aside from the varous letters to journal editors ( a very interesting read in 
themselves, but not usually peer reviewed to the same extent as an article) and 
one or two that somehow got caught in the search but really had nothing to do 
with the subject at hand (pardon the pun), the impression I got from this set 
was that it was extremely painful even with a variety of post op anesthetics.  
Then in combination with Ketamine (some time or other look up its neuropsych 
effects, real scary), which is a very powerful hallucinogen  with the other 
traumatic effects, no wonder a significant portion of cats getting declawed 
have significant behavioral problems etc.

An interesting discussion taken from wikipedia:

http://en.wikipedia.org/wiki/Ketamine

Ketamine produces effects similar to PCP and DXM. Like other dissociative 
anesthetics in low- to upper-middle dosages, its hallucinogenic effects are 
only seen against a background lacking sensory stimulation, such as darkness. 
Unlike the other well known dissociatives PCP and DXM, ketamine is very short 
acting, its hallucinatory effects lasting fifteen minutes or less when 
insufflated or injected, the total experience lasting no more than one or two 
hours. In occasional users the mind altering effects of ketamine may last for 
around 45 minutes and reduce to a mild buzz until completely sober over around 
an hour or so.
Like the other dissociative anaesthetics DXM and PCP, hallucinations caused by 
ketamine are fundamentally different from those caused by tryptamines and 
phenethylamines. At low doses, hallucinations are only seen when one is in a 
dark room with one's eyes closed, while at medium to high doses the effects are 
far more intense and obvious. These effects include changes in the perception 
of distances, relative scale, colour and durations/time, as well as a slowing 
of the visual system's ability to update what the user is seeing. There are 
reports of high-dosage users being able to see their surroundings in two sharp 
images, as if the brain is unable to merge the images each eye is sending. 
Speech often sounds unintelligible i.e. alogia, and auditory hallucinations may 
occur. At high doses sounds can be out of sync with the user's visual field.
Ketamine produces a dissociative state, characterised by a sense of detachment 
from one's physical body and the external world. At sufficiently high doses 
(e.g. 150 mg intramuscular), users may experience what is coined the "K-hole", 
a state of dissociation whose effects are thought to mimic the phenomenology of 
schizophrenia. This may include distortions in bodily awareness, such as the 
feeling that one's body is being tugged, or is gliding on silk, flying, or has 
grown very large or distended. Users often report feeling more skeletal or 
becoming more aware of their bones - the shape of their hands is also often of 
interest. Users may experience worlds or dimensions that are ineffable, all the 
while being completely unaware of their individual identities or the external 
world. Users may feel as though their perceptions are located so deep inside 
the mind that the real world seems distant (hence the use of a "hole" to 
describe the experience). Some users may not remember this part of the 
experience after regaining consciousness, in the same way that a person may 
forget a dream. Owing to the role of the NMDA receptor in long-term 
potentiation, this may be due to disturbances in memory formation. The 
"re-integration" process is slow, and the user gradually becomes aware of 
surroundings. At first, users may not remember their own names, or even know 
that they are human, or what that means. Movement is extremely difficult, and a 
user may not be aware that he or she has a body at all.
[edit]Long-term side effects

Main article: Olney's lesions
In 1989, psychiatry professor John Olney reported that ketamine caused 
reversible changes in two small areas of the rat brain. 40mg/kg resulted in 
fluid-filled bags ("vacuoles") appearing inside cells. The bags disappeared 
after several days, unless high doses of the far more toxic PCP or close 
relative MK801 were repeatedly given, in which case some cell death was seen. 
Roland Auer injected monkeys with MK801 and was unable to produce any vacuoles. 
I asked Auer in 1998 whether persons undergoing anesthesia with Ketalar were at 
risk of these changes. His reply was that he doubted that it was even a remote 
possibility because of fundamental differences in metabolism between the rat 
and human brain. Ketamine can block excito-toxicity (brain damage due to low 
oxygen, low sugar, epilepsy, trauma etc.) but it can also excite the brain at 
low doses by switching off the inhibitory system. Why isn't this damaging in 
monkeys and humans? The answer probably lies in the fact that ketamine binds to 
an increasingly wide range of different receptors as the dose level rises, and 
some of these receptors act to shut down the excitement. In humans, by the time 
a potentially toxic dose is reached, the "excitement window" has been passed 
and the drug is starting to activate other systems that switch cells off again, 
a result of ketamine's promiscuity that improves its safety relative to MK801. 
MK801 binds very specifically to N-P receptors. The other part of the 
explanation is that rats have rates of brain metabolism that are almost twice 
as high as those in humans to start with. It is because of this higher base 
rate of metabolism that ketamine causes over-excitement in rats at doses below 
those at which it activates shutdown systems.”[45][46][47]
Vutskits et al from Geneva showed that short-term exposure of cultures to 
ketamine at concentrations of > or =20 microg/ml leads to a significant cell 
loss of differentiated cells and that non-cell death-inducing concentrations of 
ketamine (10 microg/ml) can still initiate long-term alterations of dendritic 
arbor in differentiated neurons, including dendritic retraction and branching 
point elimination. They also demonstrated that chronic (>24 h) administration 
of ketamine at concentrations as low as 0.01 microg/ml can interfere with the 
maintenance of dendritic arbor architecture. These results raise the 
possibility that chronic exposure to low, subanesthetic concentrations of 
ketamine, while not affecting cell survival, could still impair neuronal 
morphology and thus might lead to dysfunctions of neural networks.[48]
Ketamine effects on horses, which where applied by the US army in Arizona 
during the 1980's proved ketamine provided horses with the faculty to jump 
notably higher than when they were not under the influence of ketamine.
There is a long list of medicines that could counteract these potential toxic 
effects, including clonidine, anticholinergics, benzodiazepines and 
barbiturates.[46][47]
On 21 June 2007 Hong Kong Medical Journal has put up a report regarding the 
misuse of 'street K'. The report suggests that long term use may result in 
damage to the liver or urinary bladder, or even acute renal failure. However, 
the researchers suspect that the damage "may be due to other toxins that the 
'street ketamine' has been contaminated with".[49]
In a study of 9 daily ketamine users, Shahani et al found "marked thickening of 
the bladder wall, a small capacity, and perivesicular stranding, consistent 
with severe inflammation. At cystoscopy, all patients had severe ulcerative 
cystitis. Biopsies in 4 patients revealed epithelial denudation and 
inflammation with a mild eosinophilic infiltrate. Cessation of ketamine use, 
with the addition of pentosan polysulfate, appeared to provide some symptomatic 
relief."[50]

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