Online ISSN : 1687-8329

    




Quick Search 
 
Author  
Year    
Title  
Vol:  

 
 
July2007 Vol.44 Issue:      2 Table of Contents
Full Text
PDF


Cognitive Impairment in Patients with Parkinson's Disease

Rashed N1, El-Sayed S1, Soltan L2, Alsherif A1, Saleh M1

Department of Neuropsychiatry, Minoufiya1, Alexandria2 Universities  



ABSTRACT

Introduction: Although Parkinson’s disease has been regarded primarily as a disorder of movement, there is considerable evidence that a substantial proportion of sufferers also show impairment of cognitive functions. The relationship between disordered movement and impaired cognitive function is of great clinical and theoretical importance. Aim of The Work: To study cognitive impairment in patients suffering from Parkinson’s disease. Patients and Methods: Thirty idiopathic Parkinson's disease patients were included. Forty three percent were males and the rest were females. Their mean age was 61.7±7.4 years. Twenty controls matching in age, sex and educational level as far as possible were selected. Two neuropsychological tests were applied to both groups: Mini-mental state examination (MMSE) and Stanford-Binnet 4th edition tests. On the basis of the results of MMSE, patients were further subdivided into two groups: those with cognitive impairment (Group A) and those without cognitive impairment (Group B). Results: Patients with Parkinson's disease showed marked impairment in attention and calculation, language, memory and perception and visuospatial function compared to normal controls. Age and Educational level played a significant role in cognitive impairment in PD patients. Cognitive impairments were found more in Akinetic-dominant type patients and PD patients not receiving L–Dopa medication, however, no significant relation to the duration of such treatment could be specified. Conclusion: There was significant cognitive impairment in patients with Parkinson's disease. MMSE was found to be very suitable, brief and quick tool in reporting cognitive impairment in PD patients. However Stanford Binnet was the tool of choice for précising the specific areas of cognitive impairment. Hence it may be used for follow up of therapeutic programs. (Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 461-471)




INTRODUCTION

 

James Parkinson's essay on the shaking palsy refers to the "unhappy sufferer", but his comment" the senses and intellect remain uninjured" was considerably less accurate.1

A compelling argument for common neurophysiological processes underlying motion and emotion is the high frequency of intellectual impairment, depression and personality changes in diseases of the basal ganglia as well as the common occurrence of motor disorders seen in schizophrenia, affective disorders, and obsessive compulsive disorder.2

PD is attributable primarily to depletion of dopamine in the basal ganglia, but the full effects of this depletion are still unknown.3 Changes in cognitive function can frequently been detected even in non demented PD patients. Specific impairments are most frequently seen in strategic cognitive abilities such as effortful recall of information, dual-process tasks, memory of temporal order, and switching of cognitive sets. These deficits are thought to be a result of impairment of the caudate outflow to the frontal lobes.2

Behavioural studies have identified patterns of cognitive deficits similar to frontal lobe dysfunction. However, the existance of an exclusive frontal-like deficit syndrome has been debated. Furthermore, deficits in tasks have been characterized that are not solely attributable to frontal lobe function alone such as impairment in probabilistic classification learning conditional.2

The relationship between disordered movement and impaired cognitive function is of great clinical and theoretical importance.4 Neuropsychiatric symptoms are important determinants of mortality and disease progression, as well as of the patients' quality of life and course of disease, caregiver distress, and nursing home admission. The exact mechanisms mediating these deficits and, particularly, the complex relationship of cognitive signs and antiparkinsonian treatment are not well understood. A clearer understanding of these mechanisms could potentially influence treatment choices, drug development and, ultimately, patient care.5

Neuropsychological deficits are not an inevitable consequence of the disease, yet the reasons underlying cognitive heterogeneity in PD are not well understood.6

 

Aim of The Work

To study cognitive impairment in patients with Parkinson's disease.

 

PATIENTS AND METHODS

 

Thirty PD patients, 51-80 years old (mean age 61.7±7.1 years) participated in this study. They included 13 males (43%) and 17 females (57%).

                A control group was assembled as a reference sample. They were 20 subjects matched in age, sex and  level of education as far as possible with the patients' group. Non of these control subject had met the dementia criteria or have had parkinsonism.

The patients were diagnosed as having PD using Parkinson's Disease Society Brain Bank Diagnostic criteria.7 They must also be free of other diseases known to affect the cognitive function.

Excluded from this study, patients with age below 30 years, those with early severe dementia with disturbance of memory, language and praxis and those having more than one affected Parkinsonian  relative.

Patients who might have atypical PD syndrome as progressive supra nuclear palsy or multiple system atrophy, cerebellar signs, early severe autonomic involvement or strictly unilateral features after 3 years were deliberately abstained.

History of stroke, cerebral tumor, traumatic brain injury, epilepsy, or psychiatric illness and/or drug intake affecting the cognitive function were quiet enough for debarring the patients from participation.

 

Each patient and control subject was subjected to:

1-            History taking.

2-      Complete physical and neurological examination including routine laboratory investigations.

3-            Brain Computerized Tomography (CT).

4-      Neuropsychological tests for assessment of cognitive functions including:

·       Mini-Mental State Examination (MMSE).8

·       Stanford-Binnet 4th edition battery which is characterized by its ability to measure all global and specific cognitive functions. It was translated into Arabic by Lois Melaka and published in 1998. It is composed of 4 main tests, which are verbal reasoning; quantitative reasoning; visual reasoning and short-term memory. The total score is considered as indicator for global cognitive functions and each test is composed of subtests, the total of them are 15 and each is an indicator for specific cognitive function.

Statistical Analysis:

Data were collected, tabulated and analyzed by SPSS version 11.0 statistical package (SPSS Inc. Chicago, Illinois, USA).Quantitative data were expressed as mean and standard deviation (X±SD). Student t-test was used to compare two groups of normally distributed variables and Mann-Whitney (U – test) for non – normally distributed variables. Qualitative data were expressed as number and percentage and analyzed by Chi-square test with or without Yale's Continuity Correction when appropriate. One-way analysis of Variance (F – test) was used for comparison of the means of more than two groups followed by LSD (least significance difference) Pos-hoch for multiple pair wise comparisons.

Level of significance was set as P – value < 0.05.

 

RESULTS

 

High statistically significant difference was shown between the patients and controls as regards the total score of MMSE. However no significant difference was present in orientation and recall (Table 1).

With the exception of verbal relation, paper cutting, quantitative reasoning and equation building tests, there was highly significant difference between patients and controls in most of the neuropsychological battery, as well as in the grand score of Stanford Binnet tests. (4th edition: The Global cognitive function) (Table 2).

According to MMSE results, parkinsonian patients were further subdivided into two group: Group A [those with cognitive impairment]: having < 24 score. They were 12 patients (40%). Group B [those without cognitive impairment] i.e. having > 24 score. They were 18 patients (80%).

 

No significant differences was found between the two groups of patients as regards gender, duration of illness and/or medication.

Patients on levodopa medication showed less cognitive impairment than those who were not and this reached statistical significance.

as regards motor function, there was a highly significant difference between patients with and those without cognitive impairment.

Patients showing dominance of bradykinesia revealed marked cognitive impairment than those showing dominance of tremors (Table 3).

                High statistical significant difference was also found between both groups as regards age, educational levels and  socioeconomic  status. (Table 3).

Non significant difference was found between both neuropsychological tools (MMSE and Stanford Binnet test) as regards vocabulary, comprehension, absurdities, verbal relation, paper cutting, quantitative, reasoning, number series, memory for digits, and equation building subtests. Non significant difference between croup B and controls was detected in the aforementioned tests (Table 4).

There was a highly statistical significant differences between patients with and those without cognitive impairment (group A and B respectively) as regards verbal reasoning, quantitative reasoning and memory tests. While non significant differences was found between both groups in the visual reasoning test.

Non significant difference was found between group B and controls as regards verbal reasoning and quantitative reasoning. On the other hand a highly significant difference was found between them in the visual reasoning and short memory tests of Stanford Binnet.


 

Table 1. Comparison of occurrence of cognitive impairment by MMSE between Parkinson's disease patients and control group.

 

MMSE

PATIENTS

n = 30

CONTROL

n = 20

T

test

P

value

Orientation

Registration

Attention & Calculation

Recall

Language

9.57±0.50

2.60±0.49

2.50±0.51

2.43±0.50

7.63±0.96

9.50±0.51

3.0±0.0

4.85±0.36

2. 45±0.51

8.50±0.51

0.45

4.39

18.97

0.11

4.12

>0.05

<0.001***

<0.001***

>0.05

<0.001***

Total score

M.M.S.E

£ 24n (%)

> 24n (%)

24.73±2.30

 

12 (40)

18 (80)

28.30±0.73

 

 

20 (100)

7.90

 

 

8.44

<0.001***

 

 

> 0.01**

Values are expressed as mean ± SD or as percentage of patients presenting with the finding.

*** =  Highly significant                         **   =  Moderately significant

 

 

Table 2. Correlation of performance of PD patients and control group in subtests of Stanford Binnet.

 

Subtests of Stanford Binnet

PATIENTS

N = 30

CONTROL

N = 20

T 

test

P

Value

Mean±SD

Mean±SD

 

 

Vocabulary test

42.50 ± 3.55

44.95 ±2.03

2.78

> 0.01**

Comprehension test

41.50 ± 6.09

46.0 ± 4.07

2.89

<0.01**

Absurdities test

49.27 ± 3.29

51.15 ± 2.20

2.24

<0.05*

Verbal relation test

36.53 ± 2.86

37.25 ± 3.27

0.81

<0.05

Pattern analysis

38.73 ± 3.39

49.35 ± 5.88

7.29

<0.001***

Copying test

41.63 ± 3.39

50.20 ± 3.60

8.01

<0.001***

Matrices test

43.87 ± 2.44

50.25 ± 2.57

8.91

<0.001***

Paper cutting test

44.53 ± 3.91

46.05 ± 5.97

1.0

<0.05

Quantitative reasoning test

42.13 ± 3.67

43.05 ± 2.01

1.01

<0.05

Number series test

45.0 ± 4.10

47.60 ± 1.98

2.98

<0.01**

Equation building

43.80 ± 3.04

44.20 ± 2.80

0.47

<0.05

Bead memory test

46.90 ± 3.75

53.20 ± 3.90

4.28

<0.001**

Memory for sentences

52.40 ± 7.02

65.90 ± 5.39

7.27

<0.001**

Memory for digits

42.57 ± 5.96

49.10 ± 4.94

4.05

<0.001**

Memory for objects

41.93 ± 4.74

50.30 ± 4.21

6.38

<0.001***

*** =  Highly significant.                                                                       * = Significant

 

Table 3. Demographic and clinical characteristics of Parkinson's disease patients with and without cognitive impairment by MMSE.

 

Variables

Parkinson's disease patients

T

test

P

Value

Group A

Group B

With cognitive impairment

Without cognitive impairment

No.                          %

No.                          %

Age (years)

 

 

 

 

Mean ± S.D

67.58±5.17

57.72±5.34

5.01

<0.001***

Range

60 – 80

50 – 66

 

 

Sex

 

 

 

 

Male

4

33.3

9

50.0

0.27

<0.05

Female

8

66.7

9

50.0

 

 

Total

12

100

18

100

 

 

Educational level

 

 

 

 

 

 

Illiterate

8

66.7

0

0.0

17.77

<0.001**

Moderate education

4

33.3

11

61.1

 

 

High education

0

0.0

7

38.9

 

 

Total

12

100

18

100

 

 

Socioeconomic status

 

 

 

 

 

 

Low

8

66.7

0

0.00

 

 

Middle

4

33.3

11

61.1

17.77

<0.001***

High

0

0.0

7

38.9

 

 

Total

12

100

18

100

 

 

L- Dopa medication

 

 

 

 

 

 

Yes

6

50.0

17

94.4

5.66

<0.05*

No

6

50.0

1

5.6

 

 

Total

12

100

18

100

 

 

Duration of treatment

 

 

 

 

Mean ± S.D

1.25±2.05

2.44±1.75

1.70

> 0.05

Median (range)

0.50 (0-6)

2(0-6)

 

 

Duration of illness

 

 

 

 

Mean±S.D

4.08±2.81

3.89±2.37

Mann-Whitney

> 0.05

Median (range)

3(1-10)

4(1-9)

0.02

 

Type of disease

 

 

 

 

Tremor dominant

0

0.0

17

94.4

22.44

< 0.001***

Akinetic dominant

12

100.0

1

5.6

 

 

Total

12

100

18

100

 

 

* = Significant.                                                                                        *** = Highly significant

 

Table 4. Comparison between performance of Parkinson's disease patients groups (with and without cognitive impairment by MMSE) and the control group in the subtests of Stanford Binnet.

 

Subtests of Stanford Binnet

Parkinson's disease patients

Controls

F
 test

P

value

 

Group A (N=12)

Group B (N=18)

Mean±SD

Mean±SD

Mean±SD

Vocabulary test

39.92±2.19

44.22±3.24

44.95±2.03

15.52

< 0.001

P1< 0.001***

P2<0.001***

P3 >0.05

Comprehension test

36.17±5.09

45.06±3.62

46.0±4.07

23.13

< 0.001

P1> 0.001***

P2<0.001***

P3 >0.05

Absurdities test

47.42±2.77

50.50±3.07

51.15±2.20

7.71

< 0.001

P1< 0.01**

P2<0.001***

P3 >0.05

Verbal relation tests

34.75±1.54

37.72±2.94

37.25±3.27

4.34

< 0.05

P1< 0.01**

P2< 0.05*

P3 > 0.05

Pattern analysis

36.92±2.81

39.44±3.26

49.35±5.88

35.98

< 0.001

P1< 0.05

P2< 0.001***

P3 > 0.001***

Copying test

41.92±4.87

41.44±3.11

50.20±3.60

30.82

< 0.001

P1> 0.05

P2< 0.001***

P3 < 0.001***

Matrices test

43.50±2.84

44.11±2.13

50.25±2.57

39.49

< 0.001

P1> 0.05

P2< 0.001***

P3 < 0.001***

Paper cutting test

42.58±0.51

45.83±4.63

46.05±5.97

2.32

> 0.05

 

Quantitative test

40.0±1.59

43.56±4.0

43.05±2.01

6.29

< 0.01

P1< 0.01**

P2< 0.01**

P3 > 0.05

Number series

41.92±2.99

47.06±3.42

47.06±1.98

17.10

< 0.001

P1< 0.001***

P2< 0.001***

P3 > 0.05

Equation building

42.0±0.0

45.0±3.46

44.2±2.80

4.34

< 0.05

P1< 0.01**

P2< 0.05*

P3 > 0.05

Bead memory

42.83±2.91

49.61±6.60

53.20±3.90

20.76

< 0.001

P1< 0.001***

P2< 0.001***

P3 > 0.05*

Memory for sentences

46.42±3.65

56.39±5.77

65.90±5.39

23.84

< 0.001

P1< 0.001***

P2< 0.001***

P3 > 0.001***

Memory for digits

39.17±2.75

44.83±6.49

49.10±4.94

13.82

< 0.001

P1< 0.01**

P2< 0.001***

P3 > 0.05

Memory for objects

39.58±3.45

43.50±4.91

50.30±4.21

25.93

< 0.001

P1< 0.05*

P2< 0.001***

P3 < 0.001***

Total score

615.1±21.8

567 – 637

678.8±39.8

637-772

728.55±25.83

682-774

50.83

< 0.001

P1< 0.001***

P2< 0.001***

P3 < 0.001***

*= Significant                                 ** = moderately significant                   *** = highly significant

P1= Between patients with & those without cognitive impairment. (Group A&B respectively)

P2= Between group A and controls.                                                        P3= Between group B and controls

Table 5. Comparison of total scores of Stanford Binnet subtest in both PD groups & controls.

 

Main 4 tests of Stanford Binnet

Group A

Group B

Controls

F
 test

P

value

 

Mean±SD

Mean±SD

Mean±SD

Verbal reasoning

158.25±10.5

177.5±10.8

179.35±7.3

21.11

< 0.001

P1< 0.001***

P2<0.001***

P3 >0.05

Visual reasoning

164.91±6.3

171.33±7.8

195±12.2

49.91

< 0.001

P1> 0.05

P2<0.001***

P3 <0.001***

Quantitative reasoning

123.91±3.6

135.61±9.5

134.85±3.8

14.11

< 0.001

P1< 0.001***

P2<0.001***

P3 >0.05

Memory tests

168±7.6

194.33±17.7

218.5±12.6

50.72

< 0.001

P1< 0.001***

P2< 0.001***

P3 < 0.001***

Grand score

615.1±21.8

678.8±39.8

728.5±25.8

56.92

< 0.001

P1< 0.001***

P2< 0.001***

P3 < 0.001***

Range

567-637

637- 772

682 – 774

 

 

*= Significant                                 ** = moderately significant                   ***= highly significant

 

 


DISCUSSION

 

                Domain-specific cognitive deficits are ubiquitous in Parkinson's disease, and although they may not be clinically apparent in all patients, they are demonstrable by neuropsychological testing.9

In the present study patients with Parkinson's disease showed significant impairment in global cognitive functions by both MMSE and Stanford Binnet tests as compared to normal controls. Twelve out of thirty (40%) patients with PD had significant cognitive impairment by MMSE (cut-off score of 24 or less). The same prevalence was also demonstrated by Paulus, et al.10 and Papapetropoulos et al.11.

On the other hand, Carman et al.12, conducted a controlled study on 103 PD patients, and found that 55% of non demented PD patients were cognitively impaired. This was relatively higher than ours. A United Kingdom based PD prevalence studies found frequencies of cognitive impairment varying between 18.5% using MMSE (cut off score 24 or less) and 41% using a cut off of 25 or less which was relatively lower than that of the present study.13

This differences could be attributed to variation in the patients selection. Demographic factors, educational level, age of onset of the disease or duration of illness, all are contributing factors to this variation.

As regards attention; This study revealed that, patients with Parkinson's disease had marked impairment in Attention and Calculation compared to normal controls. Test for sentences showed more impairment than Bead test and Digit span test. On the same line was the studies done by Brown et al.14, who reported that Parkinson’s disease has conventionally been considered to be a motor disorder, but there is growing evidence that cognition, and in particular attention, may also be impaired by the disease.

Language, was studied globally by using MMSE and specifically by Stanford Binnet neuropsychological tools. Significant impairment was found in patients with PD as compared to normal controls. Vocabulary and Comprehension tests were more impairmend than Verbal relation test. This coincided with Grossman et al.15, who proved that patients with PD can demonstrate sentence-processing deficits.   

Similarly Zgaljardic et al.16, found impaired syntactic performance in PD and attributed it in part to cognitive resource limitations (i.e. working memory and information processing speed).

As for Memory, in the present study it was found that, short term memory, visual memory, verbal memory and long term memory were affected in patients with Parkinson's disease. Working memory (memory for digits) was significantly impaired in PD patients with cognitive impairment. This agreed with Cooper et al.17, who showed that short-term memory deficit in Parkinson's disease correlated with deficits of working memory and involved attention and executive function. In another study done on 135 PD patients using MMSE and the Cambridge Cognitive Assessment–Revised (CAMCOG-R) neuropsychological tools, Athey, et al.13, found that they scored relatively poorly in expression, memory and praxis. This was in contrast to Pillon et al.18, who found that patients with Parkinson's disease might have a deficit in memory for spatial location with relative preservation of verbal memory, perceptual visuospatial and executive functions. Weintraub et al.19, in a study on sixty-three subjects (60 male, 3 female) with idiopathic PD suggested that it is possible to classify PD patients as having one of three distinct memory profiles, either unimpaired / impaired retrieval, or impaired encoding. Our results coincided more or less with, Marinus et al.20, who held a study on 85 PD patients and 75 normal controls, and found that active memory was especially impaired, whereas verbal functions were relatively spared.

Coming to Perception & Visuospatial function, PD patients in the current study were significantly impaired in tests of pattern analysis, copying test and matrices test while deterioration was not statistically significant in paper cutting test. However, their global score denoted significant impairment.

Our findings were consistent with Zgaljardic et al.16 and Marinus et al.20. The later reported that visuospatial deficits are frequently encountered in PD and that non-demented PD patients may not necessarily exhibit a pure visuospatial deficit (e.g., orientation and distance, judgment of direction, and visual analysis and synthesis) although task performance may be compromised if tests are timed and/or incorporate either a motor and/or frontal/executive element.20

Yet, the present study were in contrast to Taylor et al.21, who investigated allocentric, egocentric and right–left orientation visuospatial functions in samples of non-demented PD patients and normal controls and found the patients' response accuracy across tasks was comparable with normal controls but their reaction times were significantly prolonged.

PD patients with cognitive impairment were significantly older in age and had lower level of education than those patients with normal cognition. Thus denoting that both age and education play a significant role in cognition. Pai et al.22 studied 102 patients with PD and found that higher educational and occupational attainment was associated with reduced risk of development of cognitive decline. In the current study, it was found that the type of dominant symptom either tremor dominant or akinetic dominant was highly statistically significant in favor of the latter type denoting that cognitive impairment in PD increased when bradykinesia and rigidity were dominant. The risk factors for dementia include older age and masked facies at onset of PD, depression, levodopa-induced hallucinations and akinetic-rigid predominant features.23 Bradyphrenia may represent the cognitive analogue of bradykinesia and may, in part, reflect disruption of non-dopaminergic pathways. It represents one of features of subcortical dementia in PD together with psychomotor retardation and depression.

Correlation was found between the treatment with dopamine and the cognitive abilities of our patients. Cognitive impairment was more in patients not receiving L-dopa medication, however no significant relation to the duration of such treatment was found. Kulisevsky et al.24, stated that dopaminergic agents may enhance cognitive functions in some patients and impair them in others. De novo patients tend to improve during the first year of treatment; stable responders to oral levodopa tend to show no changes, and wearing-off responders tend to deteriorate with acute levo-dopa challenge. In contrast to the prior data, Papapetropoulos et al.11 found in their study that PD patients with cognitive impairment received higher doses of levodopa compared with the controls.

According to our results, it was found that Stanford Binnet 4th edition as a neuropsychological battery for cognitive assessment was more specific and detailed than MMSE. Both tools are comparable regarding domains of language, abstract thinking and reasoning as noted by absence of any statistically significant differences between related results. However visuospatial function, perception, attention and memory were assessed more specifically and accurately by Stanford Binnet neuropsychological tool.

 

Conclusion and Recommendations

MMSE was found to be a very suitable brief and quick tool that can be helpful in reporting cognitive impairments in patients with Parkinson disease. For more detailed data as regards  specific areas of cognitive impairment and for the sake of a specific program to be created for therapeutic purpose of each defective area Stanford Binnet is the tool of choice; although time consuming.

Detection of cognitive impairment is indispensable not only as a marker of morbidity and disease progression; but also as an indicator of the quality of life of the patient, the course of the disease, the caregiver distress and the need for nursing home admission. This denotes that by all mean professionals in this field are in great need to tackle seriously the emotional and financial burdens that is expected not only to affect the quality of life and prognosis of the disorder but also those who are around the patient. Specific therapeutic programs should be designed based on meticulous assessments according to the level of the problem and further research should be conducted to report its effectiveness.

 

REEFRENCES

 

1.      Foti DJ and Cummings JL. Neurobehavioral aspects of movement disorders. In: Watt RL, Koller WC(eds) Movement disorders: Neurologic principles and practice United States: Mc Graw Hill companies, Inc. 1998; 15-30.

2.      Cummings JL: Clinical neuropsychiatry. New York: Grune & stration, 1985.

3.      Suchowersky, Oksana, Furtado, Sarah. Parkinson's disease: etiology and treatment. Continuum: Lifelong Learning in Neurology 2004; 10(3): 15-41.

4.      Mindham RHS. Research into parkinson's disease and its relevance to understanding degenerative neurological disease. Hong Kong J Psychiatry 2002; (1): 11-14.

5.      Carbon, Maren, Marié, Rose-Marie. Functional imaging of cognition in Parkinson's disease. Current opinion in neurology 2003; 16(4): 475-480.

6.      Lewis SJ, Dove A, Robbins TW, Barker RA, Owen AM. Cognitive impairments in early Parkinson's disease are accompanied by reductions in activity in frontostriatal neural circuitry. J Neurosci, 2003; 23(15): 6351-6.

7.      Hughes A, Daniel S, Kilford L et al. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases: J Neurol Neurosurg. Psychiatry 1992; 55: 181-184.

8.      Folstein MF, Folstein SE, McHugh PR: Mini Mental State: a practical method for grading the cognitive state of patients for the clinician. J. Psychiat. Res. 1975; 12: 189-198.

9.      Emre M. What causes mental dysfunction in Parkinson’s disease?.  Mov Disord. 2003; 18(6): S63-71.

10.    Paulus K S., Magnano I, Galistu P, Agnetti V, Deriu M G., Occhineri C, Aiello I. Cognitive Function in Parkinson's Disease. Journal of Psychophysiology 2004; 18(1): 46.

11.    Papapetropoulos S., Ellul J., Polychronopoulos P., Chroni E. A registry-based, case–control investigation of Parkinson's disease with and without cognitive impairment. European journal of neurology, 2004; 11(5): 347–351.

12.    Carmen JanvinDag AarslandJan P LarsenKenneth Hugdahl.  Neuropsychological profile of patients with Parkinson's disease without dementia. Dementia and Geriatric Cognitive Disorders, 2003; 15(3): 126 – 132.

13.    Athey RJ, Porter RW, Walker RW. Cognitive assessment of a representative community population with Parkinson's disease (PD) using the Cambridge Cognitive Assessment-Revised (CAMCOG-R). Age and aging, 34(3): 268-273.

14.    Brown RG, Marsden CD. Internal versus external cues and the control of attention in Parkinson’s disease. Brain, 1988; 111: 323–45.

15.    Grossman M. Sentence processing in Parkinson's disease. Brain Cogn. 1999; 40: 387–413.

16.    Zgaljardic, Dennis J. MPhil,  Borod, et. al. A Review of the Cognitive and Behavioral Sequelae of Parkinson's Disease: Relationship to Frontostriatal Circuitry. Cognitive and behavioural neurology, 2003; 16(4): 193-210.

17.    Cooper JA, Sagar HJ, Sullivan EV. Short-term memory and temporal ordering in early Parkinson's disease: effects of disease chronicity and medication. Neuropsychologia, 31: 933-49.

18.    Pillon B, Ertle S, Deweer B, Bonnet AM, et al Memory for spatial location in 'de novo' Parkinsonian patients. Neuropsychologia, 1997; 35: 221-8.

19.    Weintnaub MD, Moberg PJ. et al Evidence for impaired encoding and retrieval memory profiles in Parkinson disease. Cognitive and behavioral neurology, 2004; 17(4): 195-200.

20.    Marinus J., Visser M., Verwey N., Verhey F., Middelkoop H., Stiggelbout A., van Hilten J. Assessment of cognition in Parkinson’s disease. Neurology, 2003; 61(9): 1222-1228.

21.    Taylor AE, Saint-Cyr JA, Lang AE. Frontal lobe dysfunction in Parkinson's disease. Brain, 1986; 109: 845–883.

22.    Pai M.-C., Chan S.-H. Education and cognitive decline in Parkinson's disease: a study of 102 patients. Acta neurologica scandinavica, 2001; 103(4): 243-247.

23.    Paulson HL and Stern MB. Clinical manifestations of Parkinson's disease. In: Watt RL, Koller WC (eds). Movement disorders: Neurologic principles and practice United States: McGraw Hill companies, Inc 1998; 13: 183-199

24.    Kulisevsky, Jaime. Role of Dopamine in Learning and Memory: Implications for the Treatment of Cognitive Dysfunction in Patients With Parkinson's Disease. Drugs& Aging, 2000; 16(5): 365-379.


 

 

 

 

 

 

 

 

 

 

 

 

 

الملخـص العربى

 

يعتبر مرض الشلل الرعاش من أكثر الأمراض التي تصيب الجهاز الحركي وقد أثبتت الدراسات أن هناك اضطراب معرفي يحدث في الكثير من حالات مرض الشلل الرعاش. ولهذا الاضطراب المعرفي أثاره البالغة على تطور المرض وعلى كفاءة الحياة بالنسبة للمريض من جهة وبالنسبة للقائمين عليه من جهة أخرى.

 

الغرض من البحث :

الغرض من هذا البحث هو تحديد نوع الاضطراب المعرفي الذي يحدث في مرض الشلل الرعاش مع تحديد نسبة حدوثه وإيجاد العلاقة بين هذه النتائج وبين العوامل المختلفة التي ترتبط بمرض الشلل الرعاش.

 

طرق البحث :

أجريت هذه الدراسة على 30 مريضا من مرضى الشلل الرعاش وتم استعمال نوعين من القياسات النفسيه باستخدام الاختبار المصغر للفحص العقلي واختبار ستانفورد بينيه الطبعة الرابعة.

 

نتائج البحث :

وقد أظهرت نتائج قياس وظائف المعرفة العامة أن أداء المرضى كان أقل من أداء المجموعة الضابطة في النواحي المعرفية العامة و كل من اختبار الفهم, تحليل النمط, النسخ, المصفوفات, سلاسل الأعداد, ذاكرة الخرز, ذاكرة الجمل, ذاكرة الأشياء في حين لم يظهر هذا الفرق في اختبارات العلاقات اللفظية, الاختبار الكمي وبناء المعادلات.

كما تم إثبات أن المرضى الذين يظهر فيهم الاضطراب المعرفي يكونون أكبر سنا من هؤلاء الذين لا يظهر فيهم مثل هذا الاضطراب. كذلك كان لمستوى التعليم تأثير معبر فى النتائج أيضا.

وقد أوضحت النتائج أن مرضى الشلل الرعاش الذين يتعاطون عقار الدوبامين أقل في الاضطراب المعرفي من هؤلاء الذين لا يتعاطون هذا العقار.

 

الخلاصة :

أن هناك اضطرابات معرفية معبرة بشكل احصائى فى مرضى الشلل الرعاش.



2008 � Copyright The Egyptian Journal of Neurology,
Psychiatry and Neurosurgery. All rights reserved.

Powered By DOT IT