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K Ray Chaudhuri

Publications and source records attributed to K Ray Chaudhuri.

26 records · Page 2Linked to original sources
PubMed2002

Serum prolactin levels in Parkinson's disease and multiple system atrophy.

The hypothalamic-pituitary axis (HPA) may be involved early in multiple system atrophy (MSA), whereas in idiopathic Parkinson's disease (IPD) its impairment seems to be correlated with motor disability. The release of prolactin (PRL) is mediated through the HPA and an increase in PRL levels is documented during stress. In this study, we investigated basal and erect PRL levels to assess whether basal PRL or changes in PRL levels after 60 degrees head-up tilt (HUT; orthostatic stress) could distinguish between MSA and IPD patients. We studied five patients with MSA on levodopa treatment, five levodopa-naive MSA patients, nine IPD patients on dopaminergic treatment, six drug-naive IPD patients and six normal individuals. PRL levels were measured in the supine position after 30 minutes rest and during 60 degrees HUT after 5 and 15 minutes. Baseline PRL values were significantly lower for patients with IPD than for those with MSA, both for levodopa-treated and naive patients ( p < 0.004, estimated decrease 55.1 %, 95 % CI from 29.4 % to 71.52 %). After orthostatic stress PRL levels were increased in healthy individuals after 15 minutes of HUT ( p = 0.044, estimated increase 11.5 %, 95 % CI from 0.4 % to 23.8 %), whereas there was no evidence for a change of PRL levels in patients with MSA or IPD after 5 and 15 minutes of HUT. We also did not find any evidence for a difference in PRL change after HUT between MSA and IPD patients. Baseline PRL levels might differentiate between early MSA and IPD, being higher in MSA. However, orthostatic stress using HUT appears unable to differentiate between MSA and IPD.

Aged↗
PubMed2002

The frequency and significance of 'striatal toe' in parkinsonism.

A striatal toe has been defined as an apparent extensor plantar response, without fanning of the toes, in the absence of any other signs suggesting dysfunction of the cortico-spinal tract. Little is known about the frequency and significance of this sign in parkinsonian syndromes. We prospectively examined 62 patients (Parkinson's disease: other akinetic-rigid syndromes=38:24) for the presence or absence of striatal toe and extensor plantar responses, as defined by Babinski. Details of the history, physical findings and investigations previously undertaken were rated and examined for their relevance to the response obtained from the hallux. Of the 62 patients, 17 patients showed an upgoing plantar response, of whom 13 (Parkinson's disease: other akinetic-rigid syndromes=7:6) had striatal toes, either unilateral (10) or bilateral (3). The remaining four patients showed a classical Babinski sign (Parkinson's disease: other akinetic-rigid syndromes=2:2). There was no lateralising relationship between lesions of the basal ganglia found on imaging and the side of the striatal toe, or the side of dyskinesias found at the time of examination. However, there appeared to be a greater frequency of dyskinesias and evidence of lesions involving the basal ganglia on imaging in patients with striatal toes compared with those who showed a plantar response other than upgoing. The possible relevance of these findings is discussed.

Aged↗
PubMed2002

The basis for day and night-time control of symptoms of Parkinson's disease.

While optimal treatment strategies are widely established for daytime treatment of Parkinson's disease (PD), nighttime problems of PD are often not adequately addressed in clinical practice. Nocturnal/sleep disturbance is common in PD and occurs due to a combination of the disease process and effect of dopaminergic and other treatments. The role of dopamine and other neuropeptides such as hypocretin is being investigated in the causation of sleep problems in PD. The impact of sleep dysfunction in PD on daytime fatigue and sleepiness is also being explored as such issues have important implications. The recently described Parkinson's disease sleep scale aims to measure the causes of sleep dysfunction in PD in a semi-quantitative manner and using this scale we have shown that sustained dopaminergic stimulation initiated at bedtime may help with improving motor symptoms at night and secondarily improve sleep and daytime functioning in PD.

Antiparkinson Agents↗
PubMed2002

Use of the dopamine agonist cabergoline in the treatment of movement disorders.

Cabergoline is an ergot-derived dopamine agonist used in the treatment of Parkinson's disease (PD). Both ergot and non-ergot-derived dopamine agonists directly stimulate dopamine receptors, unlike levodopa, which must undergo presynaptic breakdown to dopamine beforehand. Cabergoline has the longest half-life of the dopamine agonists currently available and is effective when given once-daily. It has been proposed that therapy with cabergoline may mimic physiological dopaminergic stimulation in PD by providing striatal intrasynaptic dopamine replacement. Its long half-life is likely to result in sustained rather than pulsatile dopaminergic stimulation, the preferred manner of treating PD. Placebo-controlled trials using cabergoline as an adjunctive therapy in PD have shown that it significantly reduces 'off' time, improves motor function and reduces levodopa requirements. Cabergoline has been shown to be as effective as other dopamine agonists in improving motor function as monotherapy in early PD, and a 5-year levodopa-controlled study indicates the superiority of cabergoline over levodopa in reducing dyskinesias. The efficacy of cabergoline in PD patients with nocturnal disabilities, restless leg syndrome and augmentation has also been demonstrated. Audits of the clinical efficacy of cabergoline indicate that it is well-tolerated and has an acceptable side effect profile.

Antiparkinson Agents↗
PubMed2002

'Sleep attacks' or 'unintended sleep episodes' occur with dopamine agonists: is this a class effect?

Controversial reports of sudden onset 'sleep attacks' resulting in road traffic accidents have recently been reported in patients with Parkinson's disease (PD) taking the non-ergot dopamine D(2 )/D(3) receptor agonists pramipexole and ropinirole. These reports have generated considerable debate as the concept of 'sleep attacks' is disputed amongst sleep specialists and most believe that isolated 'sleep attacks' not preceded by warning on the background of chronic sleepiness or 'unintended sleepiness' do not exist. A series of case reports suggested that this phenomenon may not be exclusive to the non-ergot dopamine agonists such as pramipexole or ropinirole and indeed may occur with most dopaminergic agents. Recent evidence suggest that a 'sleepiness' or 'hypoactivity' reaction to dopaminergic therapy may be related to underlying dopamine deficiency of PD rather than a drug effect. In this report we provide the evidence for the phenomenon being a class effect attributable to all dopamine agonists currently employed in the management of PD. Controversy surrounding excessive daytime sleepiness (EDS) in PD and the use of the Epworth Sleepiness Scale (ESS) in relation to PD is also discussed. In spite of variable reports, EDS is recognised to be common in PD and is likely to be related to both the disease process and drug therapy. Studies using multiple sleep latency tests have also reported differing results in PD although a recent study indicated that a subset of 'sleepy' patients with PD may experience pathological somnolence with resultant detrimental consequence on daytime and cognitive functions. We recommend that the issue of 'sleepiness' or 'sleep attacks' in PD should be routinely checked in all patients with PD and indirectly assessed by using either the ESS or the recently introduced Parkinson's Disease Sleep Scale. Those with reported 'sleep attacks' or 'unintended sleep episodes' and excessive daytime sleepiness while taking dopamine agonists or dopaminergic agents such as levodopa should have a review of their medication, should not be driving a car on their own and some may merit formal sleep architecture studies. The latter may identify sleep disorders such as secondary narcolepsy which may benefit from the use of a wakefulness promoting agent.

Disorders of Excessive Somnolence↗
PubMed1999

Nocturnal subcutaneous apomorphine infusion in Parkinson's disease and restless legs syndrome.

OBJECTIVES: Nocturnal disabilities leading to fragmented sleep arising from parkinsonian off period related complications are common, under-reported and are difficult to treat. In this study, we evaluate the use of nocturnal continuous subcutaneous overnight apomorphine infusion in Parkinson's disease and restless legs syndrome. METHODS: Six parkinsonian patients and 2 patients with restless legs syndrome with nocturnal disabilities refractory to conventional oral therapy were assessed using a sleep diary while on standard treatment and during nocturnal apomorphine infusion. Three patients agreed to assessments during placebo infusion with normal saline. RESULTS: Apomorphine led to a dramatic reduction of nocturnal awakenings, nocturnal off periods, pain, dystonia and nocturia in parkinsonian patients. In patients with restless legs syndrome, apomorphine reduced nocturnal discomfort, reduced leg movements and improved pain and spasm scores significantly. Placebo infusion reproduced pain, nocturnal spasms and sleep disruption. CONCLUSION: This study suggests that overnight apomorphine infusion may be effective in overcoming refractory nocturnal disabilities in selected patients with Parkinson's disease and restless legs syndrome.

Adult↗
PubMed1998

Natural history and survival of 14 patients with corticobasal degeneration confirmed at postmortem examination.

OBJECTIVE: To analyse the natural history and survival of corticobasal degeneration by investigating the clinical features of 14 cases confirmed by postmortem examination. METHODS: Patients with definite corticobasal degeneration were selected from the research and clinical files of seven tertiary medical centres in Austria, the United Kingdom, and the United States. Clinical features were analysed in detail. RESULTS: The sample consisted of eight female and six male patients; mean age at symptom onset was 63 (SD 7.7) years, and mean disease duration was 7.9 (SD 2.6) years. The most commonly reported symptom at onset included asymmetric limb clumsiness with or without rigidity (50%) or tremor (21%). At the first neurological visit, on average 3.0 (SD 1.9) years after symptom onset, the most often encountered extrapyramidal features included unilateral limb rigidity (79%) or bradykinesia (71%), postural imbalance (45%), and unilateral limb dystonia (43%). Ideomotor apraxia (64%), and to a lesser extent cortical dementia (36%), were the most common cortical signs present at the first visit. During the course of the disease, virtually all patients developed asymmetric or unilateral akinetic rigid parkinsonism and a gait disorder. No patient had a dramatic response to levodopa therapy. Median survival time after onset of symptoms was 7.9 (SD 0.7) (range, 2.5-12.5) years, and, after the first clinic visit, 4.9 (SD 0.7) (range, 0.8-10) years. Early bilateral bradykinesia, frontal syndrome, or two out of tremor, rigidity, and bradykinesia, predicted a shorter survival. CONCLUSION: The results confirm that unilateral parkinsonism unresponsive to levodopa and limb ideomotor apraxia are the clinical hallmarks of corticobasal degeneration, and only a minority of patients with corticobasal degeneration present with dementia. The study also suggests that a focal cognitive and extrapyramidal motor syndrome is indicative of corticobasal degeneration. Survival in corticobasal degeneration was shortened by the early presence of (more) widespread parkinsonian features or frontal lobe syndrome.

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