**1. Introduction**

Brain dysfunction can manifest itself either as focal laesions or mental impairment (Roach et al., 1996). In orthopedic patients, in comparison to any other group of hospitalized people, cognitive dysfunction was present more often. It included a deterioration of perception, memory, information analysis, attentional focus as well as of concentration and decreased patients' response (L. S. Rasmussen, 1998). When occurring after a surgery, the symptoms were defined as Postoperative Cognitive Dysfunction (POCD) (Newman, Stygall, Hirani, Shaefi, & Maze, 2007) and were nonspecific signs of brain disorders resulting from cellular abnormalities. Very often the dysfunction's nature was subclinical and no changes in diagnostic imaging were present (Wu, Hsu, Richman, & Raja, 2004). As a consequence, the hospitalization time was longer, the outcome and quality of life were worsened as well as prolonged medical and social assistance were necessary (Gao et al., 2005; Veering, 1999). The problem concerned up to 26% of elderly patients during the first week after a non-cardiac surgery (Rohan et al., 2005). Amongst 60-year-old patients who underwent major surgical procedures under general anesthesia lasting over 2 hours, 10% suffered from memory impairment and concentration problems for more than 3 months after the surgery. The disorder occurs twice more often in 70 – 80-year-old people in comparison to 60 – 70-yearolds (Harwood, 2000). According to statistic data, about 70% of the patients with POCD die within 5 years compared to about 35% of the patients without postoperative delirium (Fodale, Santamaria, Schifilliti, & Mandal, 2010).

All above data were alarming, but the problem seemed to be more complex. The diagnosis of POCD depends on performing a proper assessment of the cognitive function before and after the surgery through a battery of neuropsychological tests, so the incidence of POCD varies. According to the work of Blaise et al., the variability can result from nonstandardization of neuropsychological tests performed at different times of the day, lack of a control group, differences in significance levels between studies as well as from the socalled "learning effect", as when the same test is applied to the same person many times (Blaise, Taha, & Qi, 2007). Another question concerns the time at which the diagnosis of POCD was made. Different drugs administered in the perioperative period can affect patients' cognition. Thus some authors believe that the diagnosis of POCD should be made not earlier than 2 weeks after the surgery (Blaise, et al., 2007)

Postoperative Cognitive Dysfunction (POCD)

**3. Etiology of POCD** 

(Colonna, et al., 2002).

**3.1 Biomarkers of brain damage** 

time that has passed since the onset of changes.

support that observation (Fines & Severn, 2006).

postoperative cognitive disorders (Fodale, et al., 2010).

and Markers of Brain Damage After Big Joints Arthroplasty 5

was no evidence that hypoxemia is associated with the development of POCD (Fines & Severn, 2006). Some studies found that hypotension was the only intraoperative risk factor responsible for postoperative delirium (Kyziridis, 2006). However, other authors did not

Some authors discussed the role of genetic factors in the pathogenesis of neurodegenerative disorders. They found an association between the apolipoprotein ε4 (APO-ε4) allele and Alzheimer's disease (Blaise, et al., 2007), so the APO-ε4 gene could be a predictor of

The high incidence of cognitive dysfunction in orthopedic patients can result (apart from the above mentioned risk factors) from long bone fractures, prolonged immobilization, and partially from perioperative stress (Wu, et al., 2004) or a surgery technique. Colonna et al. concluded that the incidence of cerebral embolization after lower extremities arthroplasties was up to 40 – 60% (Colonna et al., 2002). Thromboembolic events played an important etiological role. There were described fatal cerebral embolizations that constituted complications accompanying long bones fractures (Riding et al., 2004), total knee replacements (Jenkins, Chung, Wennberg, Etchells, & Davey), hip arthroplasties (Fallon, Fuller, & Morley-Forster, 2001), and vertebroplasties (Scroop, Eskridge, & Britz, 2002) in which the embolic material passed into the brain through an open foramen ovale (Sukernik, Mets, & Bennett-Guerrero, 2001), although postmortem examinations did not reveal it

Biochemical tests are useful diagnostic tools in the examinations of functional brain disorders. Elevated serum concentrations of the markers of brain damage indicate that there has been a neuronal and/or glial injury. The biomarkers are released as a consequence of either transient ischemia or ultimate cell degradation, and their serum concentration depends on the localization of pathological changes, the degree of tissue damage and the

The ideal marker of brain damage should be: [1] highly specific, [2] highly sensitive, [3] released in cases of an irreversible damage to cerebral neurons only, [4] possible to detect in the blood and/or cerebrospinal fluid within a short period of time after the injury, and [5] released in well-known time sequences after the injury; furthermore, it ought to be [6] age- or sex-independent, [7] easily detectable in the blood since frequent drawing of cerebrospinal fluid samples is impractical, and [8] its concentration should be easily measureable in laboratory tests (Ingebrigtsen T). Many compounds were investigated for this purpose of founding such a marker. In the '70s, it was lactic dehydrogenase (LDH) and aspartate aminotransferase (AspAT); in the '80s, creatine kinase BB isoenzyme (CK-BB); and later, the S100B protein and neuron-specific enolase (NSE). Nowadays, glial fibrillary acidic protein (GFAP) seems most promising (Ingebrigtsen & Romner, 2003). The latter three (the S100B protein, NSE and GFAP) were the best known biomarkers of brain damage (Ingebrigtsen & Romner, 2003; L. E. Pelinka, 2004). Of these the S100B protein is thought to correspond the best

to the optimal indicator of a neuronal injury (Ingebrigtsen & Romner, 2003).
