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 »  Abstract
 »  Introduction
 »  Material and methods
 »  Results
 »  Discussion
 »  References

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Year : 2000  |  Volume : 48  |  Issue : 3  |  Page : 239-42

P300 in newly diagnosed non-dementing Parkinson's disease : effect of dopaminergic drugs.


Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

Correspondence Address:
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.

  »  Abstract

Changes in cognitive function are an integral part of the clinical presentation of Parkinson's Disease (PD). P300 potential studies in early stages of Parkinson's disease are lacking and effect of L-dopa therapy on these potentials is controversial. In this study, changes in P300 potentials in early stages of PD and effects of dopaminergic therapy were investigated. P300 waves were elicited by standard auditory 'odd ball' paradigm and were recorded before the start of therapy and 15 days, 3 and 6 months after the start of L-dopa therapy in 25 newly diagnosed patients with idiopathic PD. All patients were classified according to Hoehn and Yahr scale. Minimental status examination (MMSE) was done in all. Control group had 20 normal subjects. The P300 latency was not significantly increased in early Parkinson's disease. This latency was reduced with dopaminergic therapy on 15th day, but increased later. Implications of the data are discussed.

How to cite this article:
Prabhakar S, Syal P, Srivastava T. P300 in newly diagnosed non-dementing Parkinson's disease : effect of dopaminergic drugs. Neurol India 2000;48:239


How to cite this URL:
Prabhakar S, Syal P, Srivastava T. P300 in newly diagnosed non-dementing Parkinson's disease : effect of dopaminergic drugs. Neurol India [serial online] 2000 [cited 2020 Nov 24];48:239. Available from: https://www.neurologyindia.com/text.asp?2000/48/3/239/1529




   »   Introduction Top

Intellectual and cognitive decline is a well-known feature of Parkinson's disease. Initial frontal lobe dysfunction may progress to focal dementia of frontal lobe type or eventually to multifocal dementia in 20 to 30% of cases.[1],[2],[3] The spectrum of cognitive changes ranges from defects in attention, recent memory to that of constructional apraxia.[4] Various causes proposed for the cognitive decline in Parkinson's disease have been dopaminergic inactivation of frontocaudate cognitive system, use of anticholinergic drugs, coincidental Alzheimer's disease and the presence of Lewy body pathology.[5] Bradyphrenia, which implies slowness of thought, has been used to suggest intellectual decline in Parkinson's disease akin to bradykinesia that occurs in this disease.[6] However, others have suggested that bradykinesia and bradyphrenia are not obligatory, and a true dementia distinct from bradyphrenia does exist in this disease.[7],[8] Increasing awareness of cognitive disturbances has prompted studies of P300 in Parkinson's disease which serves as a marker of central cognitive processing. The electrophysiological studies can provide clues to the underlying pathogenesis of dementia and can help to differentiate different types of dementia and yield more homogeneous groups for therapeutic trials.[8] They can also help in prognosticating the dementing illness. In this study P300 latency was recorded in non-demented newly diagnosed cases of Parkinson's disease, who have not taken any treatment. The effect of levodopa on P300 latency was also studied.

   »   Material and methods Top

25 patients of Parkinson's disease and 25 age and sex matched controls were chosen for the study. The selected patients chosen had at least 2 of its cardinal features (tremors, rigidity, bradykinesia, postural instability) developing insidiously. Patients with symptomatic parkinsonism or widespread neurological illness were excluded. Detailed history, general and neurological examination was carried out with special reference to onset, duration, past history of drugs, trauma and motor disability as per Hoehn and Yahr scale.[9] CT/MRI scan of head was carried out in all the patients to exclude symptomatic cases. Minimental state examination (MMSE)[10] was carried out before starting therapy, and every time before P300 test was carried out after starting therapy.[10] P300 test was done on Nicolet Viking IV evoked response equipment. Auditory stimulus was used and patients were asked to concentrate and count rare stimuli. Responses were recorded from Fz, Cz and Pz electrodes according to standard 10-20 international system on the scalp, referenced to mastoid or ear lobule. Averaged response after 400 stimuli was taken; P300 latency was marked and noted, and mean of three P300 latencies was taken. This test was carried out at same time of the day every time it was done i.e. before starting dopaminergic monotherapy, after 15 days of starting treatment, and after 3 and 6 months of starting treatment. Relationship of latency with P300 dopaminergic monotherapy and cognitive state was also studied.


   »   Results Top

The patient group consisted of 25 subjects (8 females and 17 males) in the age range of 32-70 yrs with a mean of 58.2+9.86 yrs [Figure. 1]. The control group consisted of 25 patients, matched for age and sex. The mean duration of illness was 22.12+13.07 months [Figure. 2]. The Hoehn and Yahr score of the patients did not exceed 2 in majority of the patients [Figure. 3]. None of the patients at initiation was overtly demented, mean MMSE being 27.52+2.08 [Figure. 4]. In the 12 patients who completed the follow up, there was no change on MMSE though motor symptoms had shown significant improvement. P300 latencies were recorded in control group and in patients with Parkinson's disease before treatment and at 15 days, 3 months and 6 months after treatment [Table I]. There was no significant difference between the control group and patients before treatment. At 15 days and 3 months of treatment there was slight decrease in P300 though not significant. However, at 6 months of treatment, P300 latency showed a significant increase.


   »   Discussion Top

Parkinson's disease is characterized predominantly by its motor symptomatology, though cognitive defects also appear during the course of illness. These two processes, perhaps subserved by two parallel systems, tend to progress with time though not necessarily hand in hand.[11],[12] Electrophysiological studies can potentially help in establishing the extent of involvement of these two processes, their progression and the effect of drugs. They can also help to differentiate from Alzheimer's disease.[8] Studies of in Parkinson's disease have yielded mixed
P300 results. Hanch et al, in a mixed group of demented and non-demented PD patients, reported an increase in mean latency of P300.[13] In subsequent studies, P300 was found to be normal in non-demented group of patients and increased in demented group.[8],[14] However, reaction time was significantly prolonged in non-demented Parkinson's patients, suggesting that there was impairment of response selection and execution, though stimulus evaluation is preserved.[14],[15] In the present study, which included all newly diagnosed non-demented patients who had not received any treatment so far, latency was P300 normal, though they had motor disability of varying duration. These findings are consistent with that reported in an earlier study.[15]
The effect of levodopa therapy on P300 and motor disability has yielded inconsistent results. Sohn et al, found that P300 latency and motor symptoms decreased in non-demented Parkinson's patients on treatment, though there was no significant correlation.[16] These results indicated that central dopaminergic mechanisms contributed to P300, though in a different manner, as compared to motor system. In the present study at 15 days and after 3 months of levodopa therapy, P300 showed insignificant decrease but showed significant increase at 6 months although motor symptoms had shown improvement. Prasher and Findley too, in a similar group of patients, reported that the reaction time decreased after treatment, however, P300 latency increased.[15] These findings seem to be contrary to the theory of dopaminergic system contributing to genesis of P300. They argued that the adverse effects of levodopa therapy on P300 might be due to over stimulation of regions responsible for its generation rather than replacement in the depleted striatum. The findings in the present study, and that in the previous studies,[15],[16] seem to suggest that central cognitive processing is only weakly linked to the motor functions. P300, however, does provide us with a diagnostic tool for assessing the cognitive system at the onset, and at follow up of these patients. Along with other event related potentials, it can also help to differentiate from Alzheimer's type of dementia. Long-term studies may provide us with more insight into the pathogenesis of cognitive disturbances and its progression in Parkinson's disease and the effect of drugs on cognition. They may also help to serve as prognostic marker for dementia.

 

  »   References Top

1.Gotham AM, Brown RG, Marsden CD: 'Frontal' cognitive function in patients with Parkinson's disease 'on' and 'off' levodopa. Brain 1988; 11 : 299-321.   Back to cited text no. 1    
2.Lees AJ, Smith E : Cognitive deficits in the early stages of Parkinson's disease. Brain 1983; 106 : 257-270.   Back to cited text no. 2    
3.Brown RG, Marsden CD : How common is dementia in Parkinson's disease. Lancet 1984; 11 : 1262-1265.   Back to cited text no. 3    
4.Hayashi R, Hanyu N, Shindo M et al : Event related potentials, reaction time and cognitive state in patients with Parkinson's disease. Adv Neurol 1993; 60 : 429-433.   Back to cited text no. 4    
5.Brown RG, Marsden CD, Quinn N et al : Alteration in cognitive performance and affect arousal state during fluctuation in motor function in Parkinson's disease. J Neurol Neurosurg Psychiatry 1984; 47 : 454-465.   Back to cited text no. 5    
6.Mortimer JA, Pirozzolo FJ, Hansch EL et al : Relationship of motor symptoms to intellectual deficits in Parkinson's disease. Neurology 1982; 32 : 133-137.   Back to cited text no. 6    
7.Rafal RD, Posner MI, Walker JA et al : Cognition and the basal ganglia : separating mental and motor components of performance in Parkinson's disease. Brain1984; 107 : 1083-1094.   Back to cited text no. 7    
8.Goodin DS, Aminoff MJ : Electrophysiological difference between demented and non-demented patients with Parkinson's disease. Ann Neurol 1987; 21 : 90-94.   Back to cited text no. 8    
9.Hoehn MM, Yahr MD : Parkinsonism : Onset, progression and mortality. Neurology 1987; 17 : 427-442.   Back to cited text no. 9    
10.Folstein MF, Folstein SE, McHugh PR : 'Minimental state' - 14. Toda K, Tachihana H, Sugita M et al : P300 and reaction time A practical method for grading the cognitive state of patients in Parkinson's disease. J Geriatr Psychiatry Neurol 1993; for the clinician. J Psychiatr Res 1975; 12 : 189-198. 6(3) : 131-136.   Back to cited text no. 10    
11.Chia LG, Cheng LJ, Chuo LJ et al : Studies of dementia, depression, electrophysiology and cerebrospinal fluid monoamine metabolite in patients with Parkinson's disease. J Neurol Sci 1995; 133 : 73-78.   Back to cited text no. 11    
12.Prasher D, Findley L : Dopaminergic induced changes in cognitive and motor processing in Parkinson's disease : an electrophysiological investigation. J Neurol Neurosurg Psychiatry 1991; 54 : 603-609.   Back to cited text no. 12    
13.Elwan OH, Baradah OH, Madkour D et al : Parkinson's 16. Sohn YH, Kim GW, Huh K et al : Dopaminergic influences on disease, cognition and ageing. Clinical, neuropsychological, the P300 abnormality in Parkinson's disease. J Neurol Sci electrophysiological and cranial computerised tomographic 1988; 158(1) : 83-87.  Back to cited text no. 13    
14.assessment. J Neurol Sci 1996; 143 : 64-71.  Back to cited text no. 14    
15.Hanch EC, Syndulko K, Cohen SH et al : Cognition in Parkinson's disease : an event related potential perspective.  Back to cited text no. 15    

 

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