**8. Discussion**

IPB is found in both genders, with discretely higher representation in males. Our study shows that the gender representation for 32 patients with clinically confirmed diagnosis of JPB, by Brain Bank Criteria, is 18 males (56.25%) and females (43.75%). In most studies, as those of Haksma and all. (2007), Lions and all (2009); Linder and all. (2010), conducted in different periods and different populations, the results have big similarity with ours (8, 17, and 12).

In our study the average age of the respondents is 52.7 years. The youngest is only 30 years and the oldest is 78 years. The median value (50 years) shows that 16 respondents (50%) are in the age group of 50-59 years, and even 23 patients (71.87%) are older than 50 years (table 2, picture 2 from the results).

From the analyzed articles about the average beginning of IPD, dominant are those where the average beginning is in the sixth decade from life [21, 16, and 1].

Alves and all. (2009) in their epidemiological study in Norway, conducted on 554 patients with IPD, noted that the average age for beginning of symptoms manifestation of IPD is 54.3 years (this fits perfectly with the average age of our 32 respondents) [1].

Bradykinesia or the of stuntment in movements, as main from the list of cardinal symptoms according to Brain Bank Criteria of UK Parkinson's Disease (BBC-UKPCD), was present in all respondents. According to BBC-UKPCD criteria, to set the JPD diagnosis, the patient should have bradykinesia plus one of the rest cardinal symptoms such as tremor, rigidity or reduced postural reflexes. With the presence of only 2 symptoms (from which one must be bradykinesia) IPD can be confirmed.

Bradykinesia as cardinal symptom according to UPRDS, was estimated in the following way: 15 patients (47.87%) with 1; 10 (31.25%) with 2; 5 (15.62%) with 3 and only 2 respondents (6.25%) with 4 according to UPRDS scale.

Stefanie Lui and all. (2009) in their study make analysis of the development of bradykinesia as symptom in different disease stadiums. According to them, the disease progression is influenced from the bradykinesia as main cardinal symptom [19].

When our respondents are in question, in only one of them (3.12%), the lack of symptom reduced postural reflexes was confirmed and its value was 0, according to UPDRS scale. In our respondents, 75% had reduced postural reflexes, estimated with 1; 5 (15.62 %) with 2 and 1 (3.12%) were with values of 3 and 4.

Spildoren I and all. (2010), in their article described the postural instability as common and very important symptoms in IPD. In their patients, this instability is seen through partial walking instability in the initial disease stadium and as freezing phenomena in the advanced disease stadiums. According to them, the freezing phenomena are often expressed in simultaneous double activities and in the act of turning after short walking [13].

Kerstin Ziegler and all. (2010), describe festination and freezing in all 33 patients with more advanced stadium of IPD. The way they estimated festination and freezing in walking, was with 12 episodes walking capturing, in which motor block was seemed in 4 situations with 3 levels of double activities. Practically, these phenomenas are reflected in parameters expressed by measuring the number of steps of those patients, walking on special stripe and analysis on walking on distance of 10 meters. This is how you make assessment on expression of the postural instability [14].

Besides bradykinesia, as main cardinal symptom, as symptoms od IPD, are also found tremor and rigidity. We've found their presence in all our respondents (100%).

IPB is found in both genders, with discretely higher representation in males. Our study shows that the gender representation for 32 patients with clinically confirmed diagnosis of JPB, by Brain Bank Criteria, is 18 males (56.25%) and females (43.75%). In most studies, as those of Haksma and all. (2007), Lions and all (2009); Linder and all. (2010), conducted in different periods and different populations, the results have big similarity with ours (8, 17,

In our study the average age of the respondents is 52.7 years. The youngest is only 30 years and the oldest is 78 years. The median value (50 years) shows that 16 respondents (50%) are in the age group of 50-59 years, and even 23 patients (71.87%) are older than 50 years (table

From the analyzed articles about the average beginning of IPD, dominant are those where

Alves and all. (2009) in their epidemiological study in Norway, conducted on 554 patients with IPD, noted that the average age for beginning of symptoms manifestation of IPD is 54.3

Bradykinesia or the of stuntment in movements, as main from the list of cardinal symptoms according to Brain Bank Criteria of UK Parkinson's Disease (BBC-UKPCD), was present in all respondents. According to BBC-UKPCD criteria, to set the JPD diagnosis, the patient should have bradykinesia plus one of the rest cardinal symptoms such as tremor, rigidity or reduced postural reflexes. With the presence of only 2 symptoms (from which one must be

Bradykinesia as cardinal symptom according to UPRDS, was estimated in the following way: 15 patients (47.87%) with 1; 10 (31.25%) with 2; 5 (15.62%) with 3 and only 2

Stefanie Lui and all. (2009) in their study make analysis of the development of bradykinesia as symptom in different disease stadiums. According to them, the disease progression is

When our respondents are in question, in only one of them (3.12%), the lack of symptom reduced postural reflexes was confirmed and its value was 0, according to UPDRS scale. In our respondents, 75% had reduced postural reflexes, estimated with 1; 5 (15.62 %) with 2

Spildoren I and all. (2010), in their article described the postural instability as common and very important symptoms in IPD. In their patients, this instability is seen through partial walking instability in the initial disease stadium and as freezing phenomena in the advanced disease stadiums. According to them, the freezing phenomena are often expressed

Kerstin Ziegler and all. (2010), describe festination and freezing in all 33 patients with more advanced stadium of IPD. The way they estimated festination and freezing in walking, was with 12 episodes walking capturing, in which motor block was seemed in 4 situations with 3 levels of double activities. Practically, these phenomenas are reflected in parameters expressed by measuring the number of steps of those patients, walking on special stripe and analysis on walking on distance of 10 meters. This is how you make assessment on

Besides bradykinesia, as main cardinal symptom, as symptoms od IPD, are also found

in simultaneous double activities and in the act of turning after short walking [13].

tremor and rigidity. We've found their presence in all our respondents (100%).

the average beginning is in the sixth decade from life [21, 16, and 1].

years (this fits perfectly with the average age of our 32 respondents) [1].

**8. Discussion** 

2, picture 2 from the results).

bradykinesia) IPD can be confirmed.

and 1 (3.12%) were with values of 3 and 4.

expression of the postural instability [14].

respondents (6.25%) with 4 according to UPRDS scale.

influenced from the bradykinesia as main cardinal symptom [19].

and 12).

Tremor is estimated with 2, according to UPDRS scale in 18 respondents (56.25%); 10 (31.25%) with 1; 3 (9.4%) with 3 and only one patient (3.1%) we've found tremor estimated with 4.

Petra Vingensuh and all (2010) conducted examination on 25 respondents in initial stadium of IPD. In all of them, unilateral tremor pointed with bradykinesia was found, and it was possible to make diagnosis. Additionally, all these patients gained SPECT testing and in only 10% a proper finding of SPEKT was found. Lately, a number of articles are published, which through examination of cardinal secondary symptoms in patients with IPD, make analysis on their life quality. In our article, the estimation of the immensity of the clinical state was made using the UPDRS scale, which is generally accepted and applied in most scientific articles for Parkinson's disease [6].

The correlation between respondents' age and the immensity of the clinical state, estimated according to UPDRS scale, is shown in picture 26 in our results. This relation points the existence or negative correlation. Parkinson's disease has fairly difficult clinical state in younger patients and vice verse; the disease is manifested with lighter symptoms in elder patients. But, considering the coefficient value, we can conclude the correlation between these two parameters is statistically insignificant (p>0.05).

Barone P and all. (2009), this multicentrical article shows the frequency of the nonmotor signs and symptoms such as hyposmia, mood, sleeping, tiredness, perception difficulties, attention, memory capacity, erectil disfunction [3].

All these signs are examined in patients on different disease stadiums, and than analyzed to present their influence on the life of these patients.

The authors monitor 524 patients with Parkinson's disease, and they register their nonmotor symptoms and their influence on patients' life in different disease stadiums. They stated, that in younger patients the clinical state is tougher according to UPDRS, comparing to elder patients. Also, the study witnessed that disease progression is much faster in younger patients comparing to elder patients [3].

Keush SH and all. (2009), conducted their clinical examination of motor and nonmotor symptoms of Parkinson's disease in Holland. The authors developed a specific scale through which, the possibilities and capabilities for daily activities were analyzed, and according to which the degree of disease progression can be determined.

According to them, in younger patients we have faster symptoms progression, comparing to patients where the clinical state is manifested later [15].

The immensity of the clinical state of Parkinson's disease in our respondents of different gender, show that male patients have significantly tougher clinical state comparing to female patients.

Ivi Miler and Golomb AC (2010) made interesting, clinical-epidemiological study, in which is clearly shown that the disease is nearly equally manifested in two genders, but specific symptoms are more frequent in females and others in males. Motor symptoms which appear as a consequence of reduced function of dopaminerigic system, those which we often examine, are dominant in males, and only rigidity as motor symtoms and nonmotor signs are dominant in females [11].

It is assumed that this difference in manifestation by gender, most likely, is influenced by unknown hormonal mechanisms.

From the list of the neuropsychological examinations, the respondents gained: visual evoked potentials (VEP); somatosesoral evoked potentials (SSEP); caustic evoked potentials (BAEP) and electroencephalography (EEG). Generally in our 32 respondents, the most

Clinical and Genetic Aspects in Patients with Idiopathic Parkinson Disease 237

these symptoms, nonmotor and motor, develop parallel, meaning that in the early disease stadiums, all symptoms are lightly developed, no matter what they are like, while in the

Ajlin Juxel and all. (2010) in their study of 28 patients with IPD, conducted in Turkey, made multiple capturing with nuclear magnetic resonance on brain (MRI), measuring the thickness of brain callus in different brain regions. A correlation between the immensity of the clinical state, determined by UPDRS scale and the finding from MRI (measurement of the brain callus thickness), was set. The authors concluded that the thinner brain callus is,

In our study, G88C mutation in egzon 3 form SNCA genes isn't detected in our 32

Suterland GT and all (2009) in their immense study conducted on Australian population, of 331 patients with scattered form and family form of Parkinson's disease and 296 healthy people. The authors examined 11 known genes and all kinds of combinations of these genes correlations with symptoms manifestations of Parkinson's disease. They concluded that only LRRK2 gene has hardly any influence only in the family form of Parkinson's disease, while the rest genes, between which SNCA, have no influence at all in scattered Parkinson's disease manifestation in Australians, a result which fits the findings of our research [20]. Sarah Kamargos and all. (2009) made a study to evaluate the frequency and the phonotypical and genotypical manifestation in family and scattered forms of Parkinson's disease in Brazilian population. The examination was conducted on 575 patients with Parkinsonism, where the ones with IPD are 428. Mutations and polymorphisms on many different genes, typical for Parkinson's disease, such as alpha synuclein and LRRK2 gene, were examined. In the end, they concluded that there wasn't any mutation on alpha synuclein in all respondents and in only one patient with initial symptoms of IPD, a slight

Kristian Vajder and all. (2009), made immense study on 1262 patients with IPD and control group of 1881 patient. They checked the correlations between the fibroblastic growing factor 20 and alpha synuclein in patients with Parkinson's disease. They examined their correlations on 9 brains on deceased patients, which were previously diagnosed with IPD. The authors concluded that the role of alpha synuclein in Parkinson's disease is

[1] Alves G, Muller B,Herlofson K. Incidence of Parkinson's disease in Norway. The Norwegian Park West study. J Neural Neurosurgery Psychiatry 2009; 80: 851–857 [2] Aylin Yucel, Ozge Yilmaz Kusbeci. Magnetic resonance imaging findings of shoulders in

[3] Barone P, Antonini A, Colosimo C, et al. The PRIAMO study: A multicenter assessment

[4] Chul Hyoung Lyoo, Young Hoon Ryu, Myung Sik Lee. Topographical distribution of

[5] Christian Wider, Justus C. Dachsel, Alexandra I. Soto et al. FGF20 and Parkinson's

of nonmotor symptoms and their impact on quality of life in Parkinson's disease.

cerebral cortical thinning in patients with mild Parkinson's disease without

disease: No evidence of association or pathogenicity via α-synuclein expression.

undisputable, but the changes in sequences in this gene, were negative [5].

Parkinson's disease. Mov Disord 2010; 25 (15): 2524-2530.

respondents with IPD. The same happens with G209A in egzon 4 form SNCA gene.

more advanced stadiums, all symptoms are expressed and visible [10].

the more developed the clinical state of patients with IPD is [2].

mutation of LRRK2 gene, was found [18].

Mov Disord 2009; 24: 1641–1649.

Mov Disord 2009; 24 (3): 455-9.

dementia. Mov Disord 2010; 25 (4): 496-499.

**9. References** 

findings for evoked potentials (VEP, SSEP and BAEP) are proper. Proper VEP is found in 29 respondents (90.6%); prolonged latencies and low-volted responses are found in 2 (6.3%) and only in 1 respondent (3.1%), the finding is with low-volted response.

SSEP is with proper finding in 30 respondents (93.8%) and low-volted responses are found in 2 (6.2%). Proper BAEP finding is found in 22 (68.72%) and low-volted different components are found in 10 (31.25%).

In our patients, neuroimaging examination (CT and MRI of brain) are made; 37.5% have proper results; in 34.4% of them discrete cortical reduced changes are found and in 28.1% the pathological process is manifested with global cortical reduced changes.

Doppler color sonography on extra cranial blood vessels, shows proper finding in 62.5% of the respondents; in 21.9% lightly expressed intimacy and proper chemo dynamic parameters are found; in 15.6% of our patients have arteriosclerotical changes of the caroted blood vessels.

Lio CH and all. (2010) made a study on 84 patients with IPD, without dementia signs. They made several short capturing with MRI of brain, examining the regions which are most often damaged in these patients. Patients with medium developed clinical state were selected. They also had plenty symptoms and the exact regions which influenced the domination on specific motor and nonmotor symptoms, were determinated. Dementia as a symptom was excluded [4].

Table 11a and 11b from our results, presents the results from the neuropsychological testing. Proper cognitive capacities of testing were found only in 3 patients with IPD. Between the patients dominant are those with depression and initial reduced cognitive capacities (34.4%), as well as 31.2% with global reduced cognitive capacities.

According to the frequency of occurrence, next is the finding of depression and global reduced cognitive capacities, found in 9.4% of our respondents.

The rest findings of the neuropsychological testing: depression in behavior, anxiety in behavior, initial reduced cognitive capacities; depression and anxiety in behavior, as well as the mutual presence of depression and anxiety in behavior and initial reduced cognitive capacities are found only in 1 patient with IPD.

Lately, in different magazines and congresses, scientists try to prove the correlation between the IPD and depression as secondary symptom, as well as, dementia, found in high percent of patients with Parkinson's disease.

Ivi N Miler and Golumb AC (2010) made interesting clinical and epidemiological study, where they proved that the disease is nearly equally manifested in both genders. But, certain symptoms more often appear in females and other in males. Etiopathogenetical mechanisms for these symptoms division, is still unknown, but it is assumed that the hormonal status influences on manifestation of these symptoms. Consequently, the nonvoter symptoms (mood, hyposmia, sleeping, attention, memory, perception difficulties and depression) are dominant in females [11].

Huijuan Li and all. (2010), made a study on 82 Chinese patients, 46 males and 36 females with IPD, which lasted 18 months. Patients were on average age of 65 years. Generally, they examined the motor signs such as: mood, sleeping, depression, attention, memory capacity and perception disorder. To determinate the degree of disease, the authors used UPDRS scale. Then using a special scale for determination of nonmotoral symptoms development, they determined the degree of these symptoms. They concluded that there is a positive correlation between the development of the nonmotor and psychological symptoms in relation to the development of motor signs of the disease, according to UPDRS. Actually, all these symptoms, nonmotor and motor, develop parallel, meaning that in the early disease stadiums, all symptoms are lightly developed, no matter what they are like, while in the more advanced stadiums, all symptoms are expressed and visible [10].

Ajlin Juxel and all. (2010) in their study of 28 patients with IPD, conducted in Turkey, made multiple capturing with nuclear magnetic resonance on brain (MRI), measuring the thickness of brain callus in different brain regions. A correlation between the immensity of the clinical state, determined by UPDRS scale and the finding from MRI (measurement of the brain callus thickness), was set. The authors concluded that the thinner brain callus is, the more developed the clinical state of patients with IPD is [2].

In our study, G88C mutation in egzon 3 form SNCA genes isn't detected in our 32 respondents with IPD. The same happens with G209A in egzon 4 form SNCA gene.

Suterland GT and all (2009) in their immense study conducted on Australian population, of 331 patients with scattered form and family form of Parkinson's disease and 296 healthy people. The authors examined 11 known genes and all kinds of combinations of these genes correlations with symptoms manifestations of Parkinson's disease. They concluded that only LRRK2 gene has hardly any influence only in the family form of Parkinson's disease, while the rest genes, between which SNCA, have no influence at all in scattered Parkinson's disease manifestation in Australians, a result which fits the findings of our research [20].

Sarah Kamargos and all. (2009) made a study to evaluate the frequency and the phonotypical and genotypical manifestation in family and scattered forms of Parkinson's disease in Brazilian population. The examination was conducted on 575 patients with Parkinsonism, where the ones with IPD are 428. Mutations and polymorphisms on many different genes, typical for Parkinson's disease, such as alpha synuclein and LRRK2 gene, were examined. In the end, they concluded that there wasn't any mutation on alpha synuclein in all respondents and in only one patient with initial symptoms of IPD, a slight mutation of LRRK2 gene, was found [18].

Kristian Vajder and all. (2009), made immense study on 1262 patients with IPD and control group of 1881 patient. They checked the correlations between the fibroblastic growing factor 20 and alpha synuclein in patients with Parkinson's disease. They examined their correlations on 9 brains on deceased patients, which were previously diagnosed with IPD. The authors concluded that the role of alpha synuclein in Parkinson's disease is undisputable, but the changes in sequences in this gene, were negative [5].

#### **9. References**

236 Neuroimaging for Clinicians – Combining Research and Practice

findings for evoked potentials (VEP, SSEP and BAEP) are proper. Proper VEP is found in 29 respondents (90.6%); prolonged latencies and low-volted responses are found in 2 (6.3%)

SSEP is with proper finding in 30 respondents (93.8%) and low-volted responses are found in 2 (6.2%). Proper BAEP finding is found in 22 (68.72%) and low-volted different

In our patients, neuroimaging examination (CT and MRI of brain) are made; 37.5% have proper results; in 34.4% of them discrete cortical reduced changes are found and in 28.1%

Doppler color sonography on extra cranial blood vessels, shows proper finding in 62.5% of the respondents; in 21.9% lightly expressed intimacy and proper chemo dynamic parameters are found; in 15.6% of our patients have arteriosclerotical changes of the caroted

Lio CH and all. (2010) made a study on 84 patients with IPD, without dementia signs. They made several short capturing with MRI of brain, examining the regions which are most often damaged in these patients. Patients with medium developed clinical state were selected. They also had plenty symptoms and the exact regions which influenced the domination on specific motor and nonmotor symptoms, were determinated. Dementia as a

Table 11a and 11b from our results, presents the results from the neuropsychological testing. Proper cognitive capacities of testing were found only in 3 patients with IPD. Between the patients dominant are those with depression and initial reduced cognitive capacities

According to the frequency of occurrence, next is the finding of depression and global

The rest findings of the neuropsychological testing: depression in behavior, anxiety in behavior, initial reduced cognitive capacities; depression and anxiety in behavior, as well as the mutual presence of depression and anxiety in behavior and initial reduced cognitive

Lately, in different magazines and congresses, scientists try to prove the correlation between the IPD and depression as secondary symptom, as well as, dementia, found in high percent

Ivi N Miler and Golumb AC (2010) made interesting clinical and epidemiological study, where they proved that the disease is nearly equally manifested in both genders. But, certain symptoms more often appear in females and other in males. Etiopathogenetical mechanisms for these symptoms division, is still unknown, but it is assumed that the hormonal status influences on manifestation of these symptoms. Consequently, the nonvoter symptoms (mood, hyposmia, sleeping, attention, memory, perception difficulties and depression) are

Huijuan Li and all. (2010), made a study on 82 Chinese patients, 46 males and 36 females with IPD, which lasted 18 months. Patients were on average age of 65 years. Generally, they examined the motor signs such as: mood, sleeping, depression, attention, memory capacity and perception disorder. To determinate the degree of disease, the authors used UPDRS scale. Then using a special scale for determination of nonmotoral symptoms development, they determined the degree of these symptoms. They concluded that there is a positive correlation between the development of the nonmotor and psychological symptoms in relation to the development of motor signs of the disease, according to UPDRS. Actually, all

and only in 1 respondent (3.1%), the finding is with low-volted response.

the pathological process is manifested with global cortical reduced changes.

(34.4%), as well as 31.2% with global reduced cognitive capacities.

reduced cognitive capacities, found in 9.4% of our respondents.

capacities are found only in 1 patient with IPD.

of patients with Parkinson's disease.

dominant in females [11].

components are found in 10 (31.25%).

blood vessels.

symptom was excluded [4].


**13** 

*Brazil* 

**New Insights for a Better** 

**Understanding of the Pusher Behavior:** 

**From Clinical to Neuroimaging Features** 

*University of Sao Paulo School of Medicine at Ribeirao Preto* 

Taiza E.G. Santos-Pontelli, Octavio M. Pontes-Neto and Joao P. Leite

Disorders of postural balance are common in patients with encephalic lesions. According Tyson et al. (Tyson et al., 2006), around 80% of patients experiencing their first cerebrovascular event have static or dynamic postural imbalance. Historically, the first description of postural balance dysfunction in stroke patients dates back to more than one hundred years ago. In 1909, Beevor described the occasional lack of lateral balance in stroke patients that cause them to fall towards their contralesional side due to their paresis (Beevor, 1909). Later, Brunnstrom reported the 'listing phenomenon' as a list toward the affected side that patients cope by climbing onto something with their nonparetic hand to prevent listing

In 1968, a tendency to fall towards the lesion side and lateropulsion were described by Bjerver and coworkers in patients with Wallenberg's syndrome due to dorsolateral medullary infarction (Bjerver &Silfverskiold, 1968). These patients also presented with transient ocular tilt reaction and ipsiversive deviations of the subjective vertical, which indicate a pathological shift in the internal representation of the gravitational vector

Another postural imbalance observed in patients with encephalic lesions is thalamic astasia. According to Masdeu and Gorelick, this disorder is characterized by the inability to maintain an unsupported upright posture even without paresis or sensory or cerebellar deficits.8 When asked to sit up, patients with this disorder use the unaffected arm to pull themselves up (Masdeu & Gorelick, 1988). This behavior could be explained in part by a vestibular tone imbalance in the roll plane, especially since skew deviation was included as

As opposed to all other syndromes and phenomena described above, the pusher behavior (PB) is characterized by actively pushing away from the nonparetic side (Davies, 1985). Moreover, patients with PB lean to the side opposite the lesion and strongly resist any attempt at passive correction of their tilted body while sitting or standing. In the most severe cases, this resistance occurs even in a supine position (Pedersen et al., 1996; Lafosse et al., 2005). Such patients report a fear of falling towards their ipsilesional side (Davies, 1985; Pedersen et al., 1996; Lafosse et al., 2005) and are not aware that their active pushing is counterproductive and makes it impossible for them to stand without assistance (D'Aquila

(Dieterich &Brandt, 1992; Brandt &Dieterich, 2000; Dieterich, 2007).

a feature of the syndrome (Brandt & Dieterich, 2000; Dieterich, 2007).

**1. Introduction** 

(Brunnstrom, 1970).

