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Parkinsn Current Topics

Abstracts Authored or Co-authored by Dr. P.A. Kempster through 2009

Other related abstracts to topic

1. Mov Disord. 2009 Nov 4. [Epub ahead of print]

Longitudinal study of the levodopa motor response in Parkinson's disease:
Relationship between cognitive decline and motor function.

Alty JE, Clissold BG, McColl CD, Reardon KA, Shiff M, Kempster PA.

Neurosciences Department, Monash Medical Centre, Clayton, Victoria, Australia.

In this prospective study of 34 patients with Parkinson's disease (PD),
measurements of the short duration levodopa motor response have been performed
every 3 years in defined off states. The mean time from initiation of levodopa
treatment was 14.8 years, and 17 patients survived to the latest assessment
stage. Off phase motor function worsened at a yearly rate of 2.2% of the maximum 
disability score. The magnitude of the levodopa response is well preserved as the
disease progresses, and patients who developed motor fluctuations maintained
better on phase motor function than nonfluctuators (P = 0.01). Ten patients, of
whom 5 survive, developed dementia. There was no difference in pretreatment
disability or initial levodopa response between demented and nondemented
subjects. However, dementia was associated with worse on and off motor disability
scores after 11 and 14 years (P < 0.001), and a smaller levodopa response
magnitude after 14 years (P = 0.008). The plot of sequential scores shows the
association between cognitive decline and accelerating increase in motor
disability. This suggests that the advanced phase of PD, when Lewy body pathology
involves the cerebral cortex, progresses in an exponential rather than linear
fashion. (c) 2009 Movement Disorder     Society.

PMID: 19890972 [PubMed - as supplied by publisher]


2. Brain. 2009 Nov;132(Pt 11):2947-57. Epub 2009 Sep 16.

A clinico-pathological study of subtypes in Parkinson's disease.

Selikhova M, Williams DR, Kempster PA, Holton JL, Revesz T, Lees AJ.

Queen Square Brain Bank for Neurological Disorders and Institute of Neurology,
University College, London, UK.

We have carried out a systematic review of the case files of 242 donors with
pathologically verified Parkinson's disease at the Queen Square Brain Bank for
Neurological Disorders in an attempt to corroborate the data-driven subtype
classification proposed by Lewis and colleagues (Heterogeneity of Parkinson's
disease in the early clinical stages using a data driven approach. J Neurol
Neurosurg Psychiatry 2005; 76: 343-8). Cases were segregated into earlier disease
onset (25%), tremor dominant (31%), non-tremor dominant (36%) and rapid disease
progression without dementia (8%) subgroups. We found a strong association
between a non-tremor dominant disease pattern and cognitive disability. The
earlier disease onset group had the longest duration to death, and greatest delay
to the onset of falls and cognitive decline. Patients with a tremor dominant
disease pattern did not live significantly longer than non-tremor dominant
patients and showed no difference in mean time to onset of falls and
hallucinations. Rapid disease progression was associated with older age, early
depression and early midline motor symptoms, and in 70% of the cases, tremulous
onset. The non-tremor dominant subgroup had a significantly higher mean
pathological grading of cortical Lewy bodies than all other groupings (P < 0.05) 
and more cortical amyloid-beta plaque load and cerebral amyloid angiopathy than
early disease onset and tremor dominant groups (P = 0.047). An analysis of cases 
with pathologically defined neocortical Lewy body disease confirmed the link
between bradykinetic onset, cognitive decline and Lewy body deposition in the
neocortex. Although neuropathological examination failed to distinguish the other
subtypes, the classification scheme was supported by an analysis of clinical data
that were independent of the basic subgroup definitions.

PMID: 19759203 [PubMed - in process]


3. Brain. 2008 May;131(Pt 5):1362-72. Epub 2008 Apr 2.

Clinical outcomes of progressive supranuclear palsy and multiple system atrophy.

O'Sullivan SS, Massey LA, Williams DR, Silveira-Moriyama L, Kempster PA, Holton
JL, Revesz T, Lees AJ.

Reta Lila Weston Institute of Neurological Studies, University College London,
London, UK.

Prognostic predictors have not been defined for progressive supranuclear palsy
(PSP) and multiple system atrophy (MSA). Subtypes of both disorders have been
proposed on the basis of early clinical features. We performed a retrospective
chart review to investigate the natural history of pathologically confirmed cases
of PSP and MSA. Survival data and several clinically relevant milestones, namely:
frequent falling, cognitive disability, unintelligible speech, severe dysphagia, 
dependence on wheelchair for mobility, the use of urinary catheters and placement
in residential care were determined. On the basis of early symptoms, we
subdivided cases with PSP into 'Richardson's syndrome' (RS) and
'PSP-parkinsonism' (PSP-P). Cases of MSA were subdivided according to the
presence or absence of early autonomic failure. Sixty-nine (62.7%) of the 110 PSP
cases were classified as RS and 29 (26.4%) as PSP-P. Of the 83 cases of MSA, 42
(53.2%) had autonomic failure within 2 years of disease onset. Patients with PSP 
had an older age of onset (P < 0.001), but similar disease duration to those with
MSA. Patients with PSP reached their first clinical milestone earlier than
patients with MSA (P < 0.001). Regular falls (P < 0.001), unintelligible speech
(P = 0.04) and cognitive impairment (P = 0.03) also occurred earlier in PSP than 
in MSA. In PSP an RS phenotype, male gender, older age of onset and a short
interval from disease onset to reaching the first clinical milestone were all
independent predictors of shorter disease duration to death. Patients with RS
also reached clinical milestones after a shorter interval from disease onset,
compared to patients with PSP-P. In MSA early autonomic failure, female gender,
older age of onset, a short interval from disease onset to reaching the first
clinical milestone and not being admitted to residential care were independent
factors predicting shorter disease duration until death. The time to the first
clinical milestone is a useful prognostic predictor for survival. We confirm that
RS had a less favourable course than PSP-P, and that early autonomic failure in
MSA is associated with shorter survival.

PMID: 18385183 [PubMed - indexed for MEDLINE]


4. Brain. 2008 Sep;131(Pt 9):2520-5. Epub 2008 Feb 20.

John Ruskin's relapsing encephalopathy.

Kempster PA, Alty JE.

Neurosciences Department, Monash Medical Centre, Clayton, Victoria, Australia.
peter.kempster@southernhealth.org.au

John Ruskin (1819-1900) is chiefly remembered for his works on painting and
architecture, and for his powerful and original prose style. In middle age, he
suffered recurring episodes of delirium with visual hallucinations and delusions.
At about the same time, his writing developed a disjointed polemical character,
with cryptic and intemperate elements that disorientated some readers. The nature
of Ruskin's 'madness' is a key to understanding his later writing career but the 
psychiatric explanations given by many of his literary biographers seem
unsatisfactory. Ruskin left numerous clues about the illness in his diaries,
correspondence and publications. It is likely that he had a relapsing-progressive
neurological disorder with neuropsychiatric manifestations. It could have been a 
fluctuating metabolic or immunological encephalopathy, but the diagnosis that
best fits the time course of his illness and the prior history of mood disorder
and of migraine with aura is Cerebral Autosomal Dominant Arteriopathy with
Subcortical Infarcts and Leukoencephalopathy (CADASIL). Whatever the pathology,
its first effects on frontal lobe function may have actually enhanced Ruskin's
creative energy for a long time before stepwise cognitive impairment degraded his
ability to write.

PMID: 18287121 [PubMed - indexed for MEDLINE]


5. J Clin Neurosci. 2008 Apr;15(4):379-81. Epub 2008 Feb 14.

The Lhermitte phenomenon: variant forms and their significance.

Kempster PA, Rollinson RD.

Neurosciences Department, Monash Medical Centre, 246 Clayton Road, Clayton,
Victoria 3168, Australia. peter.kempster@southernhealth.org.au

Typical Lhermitte phenomenon (tingling sensations moving down the limbs or trunk 
on neck flexion) is a sign of intrinsic spinal cord pathology, most commonly
cervical spinal cord demyelination. The phenomenon has several variant forms, and
each has a different pathological significance. A delayed typical Lhermitte
phenomenon can follow contusion of the spinal cord from neck trauma. Reverse
Lhermitte phenomenon induced by neck extension is usually produced by extrinsic
compression of the cervical spinal cord. Upward moving paraesthesia with neck
flexion (inverse Lhermitte phenomenon) is relatively rare, and can be a sign of
myelopathy from nitrous oxide inhalation.

PMID: 18280165 [PubMed - indexed for MEDLINE]


6. Neurology. 2007 Jul 31;69(5):482-5.

A new look at James Parkinson's Essay on the Shaking Palsy.

Kempster PA, Hurwitz B, Lees AJ.

Neurosciences Department, Monash Medical Centre, Clayton, Victoria, Australia.
peter.kempster@yahoo.co.uk

James Parkinson's Essay on the Shaking Palsy, published in 1817, represents a
landmark in the development of writing about neurologic disorders. Parkinson was 
an astute clinician-investigator, and his wide scientific interests and ideas on 
social advancement in many ways typified the spirit of the Age of Enlightenment. 
Our commentary on the text of his essay identifies important sources of its
originality: the particular way in which Parkinson collected and categorized
clinical material, his use of a field neurology method to identify affected
individuals, and his skills as a narrative writer. Although the essay belongs to 
an older tradition of disease classification, it also anticipates the modern
neurologist's reliance on accurate clinical description and natural history in
establishing a diagnosis.

PMID: 17664408 [PubMed - indexed for MEDLINE]


7. Brain. 2007 Aug;130(Pt 8):2123-8. Epub 2007 Jun 24.

Patterns of levodopa response in Parkinson's disease: a clinico-pathological
study.

Kempster PA, Williams DR, Selikhova M, Holton J, Revesz T, Lees AJ.

Queen Square Brain Bank for Neurological Disorders and Institute of Neurology,
University College, London, UK.

Patients with Parkinson's disease who develop disabling levodopa-induced motor
fluctuations have a stronger therapeutic response than those who experience a
more modest but stable response. A difference in the histopathological lesion
between the two groups might be responsible. Case records from 97 patients with
pathologically proven Parkinson's disease were reviewed to determine the pattern 
of levodopa response. Pathological findings for fluctuating and non-fluctuating
cases were compared. Patients with motor fluctuations had a younger age of onset 
and longer disease course (P < 0.001), although mean age at death was almost the 
same. Four milestones of advanced disease (frequent falls, visual hallucinations,
cognitive disability and need for residential care) occurred at a similar time
from death in each group; this interval was not proportionate to the disease
duration. There were no significant differences in the severity or distribution
of Lewy body or other pathologies. Irrespective of the pattern of levodopa
response, patients reach a common pathological endpoint at a similar age, and the
duration and manifestations of end-stage disease are alike. A non-linear or
exponential time relationship may govern the late clinical and pathological
progression of Parkinson's disease.

PMID: 17586867 [PubMed - indexed for MEDLINE]


8. Mov Disord. 2006 Dec;21(12):2116-21.

Longitudinal study of the motor response to levodopa in Parkinson's disease.

Clissold BG, McColl CD, Reardon KR, Shiff M, Kempster PA.

Neurosciences Department, Monash Medical Centre, Melbourne, Australia.

In this prospective study of 34 patients with Parkinson's disease, measurements
of the short duration levodopa motor response have been performed in defined off 
states at 3 yearly intervals over a mean period of 11.4 years from the point of
commencement of levodopa treatment. Twenty-two patients were still available for 
study; 10 had died and 2 were lost to follow-up. The levodopa motor response
amplitude increases over the first 5 years of treatment, and thereafter, on and
off scores worsen in parallel with conservation of the response. Patients who
developed motor fluctuations within the first 5 years of treatment had, on
average, a stronger response to levodopa with significantly better on phase motor
function (P = 0.003). Although the proportion of "midline" motor disability
(affecting gait, balance, and cranial motor function) increases with time, these 
deficits do not actually become unresponsive to levodopa. Patients who developed 
dementia had a significantly more rapid decline in motor function. The latest
graph of serial scores for the whole cohort shows an upward curving or
exponential increase in motor disability after the first decade of treatment.
Applying a notional untreated disability line to this graph--an estimate of the
disability that would have accrued if drugs had never been given--we suggest that
the long-duration response to levodopa eventually runs down with disease
progression. Copyright 2006 Movement Disorder     Society.

PMID: 17029259 [PubMed - indexed for MEDLINE]


9. J Clin Neurosci. 2007 Jul;14(7):696-700. Epub 2006 May 2.

Sporadic encephalitis lethargica.

Raghav S, Seneviratne J, McKelvie PA, Chapman C, Talman PS, Kempster PA.

Neurosciences Department, Monash Medical Centre, 246 Clayton Road, Clayton 3168, 
Victoria, Australia.

Three women (aged 21-36 years) developed acute illnesses that were similar to
epidemic encephalitis lethargica. Each presented with a neuropsychiatric
disturbance that was succeeded by pyrexia, a fluctuating conscious state and
involuntary movements including oculogyria. Cerebrospinal fluid examination
showed a predominantly lymphocytic pleocytosis (64-120x10(6) cells/L) and
oligoclonal bands were detected in two cases. Two patients died, while the third 
made a gradual recovery. Post-mortem examination in the two fatal cases showed
changes of lymphocytic meningitis and focal diencephalic lymphocytic
infiltration, although these changes were mild relative to the effects of the
clinical illness. The diagnosis of sporadic encephalitis lethargica relies on
identifying shared clinical features with the past epidemic disease plus
circumstantial evidence of immunological activity from laboratory investigations 
and some tests of exclusion of other disorders.

PMID: 16647855 [PubMed - indexed for MEDLINE]


10. J Clin Neurosci. 2006 Apr;13(3):319-21. Epub 2006 Mar 20.

Staying on the surface.

Kempster PA.

Neurosciences Department, Monash Medical Centre, 246 Clayton Road, Clayton,
Victoria 3168, Australia. peter.kempster@southernhealth.org.au

Every neurologist needs to develop an effective technique to diagnose and manage 
non-organic disorders, although there are different ways to go about it. The
complex relationship that exists between functional and organic illness is an
inescapable theme in daily neurological practice. Usually, it is better to read
these case stories by examining their surface detail rather than to try to
understand their psychological depth.

PMID: 16546393 [PubMed - indexed for MEDLINE]


11. J Clin Neurosci. 2006 Feb;13(2):178-80. Epub 2006 Feb 3.

Looking for clues.

Kempster PA.

Neurosciences Department, Monash Medical Centre, 246 Clayton Road, Clayton,
Victoria, 3168, Australia. peter.kempster@southernhealth.org.au

At certain moments in clinical practice, one can seem to possess the powers of a 
Sherlock Holmes to search out clues and deduce the diagnosis. Many neurologists
are aware of links between the workings of detective fiction and the methods of
problem-solving in neurological cases. One similarity concerns the professional
counterpart of the conventional detective story, the single case report.

PMID: 16459091 [PubMed - indexed for MEDLINE]


12. J Clin Neurosci. 2006 Jan;13(1):14-7.

Reading a story.

Kempster PA.

Neurosciences Department, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 
3168, Australia. peter.kempster@southernhealth.org.au

Case delineation in clinical medicine is the technique of creating a narrative
that allows the appropriate scientific knowledge to be brought to bear.
Neurologists get to be good at this type of story reading and telling from
dealing with clinical stories which are relatively long and complicated. These
skills are evident whenever working neurologists gather to discuss case material,
or when studying their written clinical communications. The purpose of the
article is to analyze this aspect of everyday neurological practice by looking at
some of the general principles of story telling and appreciation.

PMID: 16410193 [PubMed - indexed for MEDLINE]


13. Mov Disord. 2004 Jan;19(1):105-6.

Michael J. Fox and his Parkinson's disease.

Kempster PA.

Neurosciences Department, Monash Medical Centre, Melbourne, Australia.

Michael J. Fox was a popular and successful film and television comic actor who
developed Parkinson's disease at the age of 29 years. His recently published
book, Lucky Man, structured around the story of his Parkinson's disease, is an
amusing, briskly paced yet introspective memoir that covers the first 40 years of
his life. Although quite anecdotal, it contains interesting observations on the
preclinical phase of the disorder, evolution of motor fluctuations, and tactics
for pharmacological treatment. Copyright 2003 Movement Disorder     Society

PMID: 14743369 [PubMed - indexed for MEDLINE]


14. J Clin Neurosci. 2003 May;10(3):394.

Re: Basilar invagination and Chiari malformation associated with cerebellar
atrophy: report of two treated cases.

Kempster PA, Pullar MJ.

Comment on:
    J Clin Neurosci. 2002 Mar;9(2):194-6.

PMID: 12763358 [PubMed - indexed for MEDLINE]


15. Mov Disord. 2002 Nov;17(6):1227-34.

Motor response to levodopa and the evolution of motor fluctuations in the first
decade of treatment of Parkinson's disease.

McColl CD, Reardon KA, Shiff M, Kempster PA.

Neurosciences Department, Monash Medical Centre, Melbourne, Australia.

Thirty-four patients with Parkinson's disease were followed for a mean period of 
8 years from the time of initiation of levodopa medication. Levodopa response was
charted from the starting point of pharmacological treatment to give a
longitudinal point of view of the changes that evolve as the disease progresses. 
Objective measurements of the motor response to levodopa test-doses were made at 
approximately three yearly intervals. Motor fluctuations developed in 58% of the 
patient group after a mean treatment period of 35 months. Dyskinesia developed in
parallel with fluctuations but appeared on average 7 months before symptomatic
wearing-off effects of levodopa doses. The patients with motor fluctuations had
significantly better responses to levodopa. By contrast, nonfluctuators were more
prone to develop increasing midline motor disability affecting speech, gait and
balance. Comparison of test-dose and pretreatment scores suggested that a
substantial long-duration response to levodopa remains after many years of
treatment, and that lateralized motor deficits show a stronger long duration
response than midline ones. Motor fluctuations are a consequence of disease
progression but their early development is, on balance, associated with better
long-term functional ability because these patients have the greater capacity to 
respond to pharmacological treatment. Copyright 2002 Movement Disorder     Society

PMID: 12465061 [PubMed - indexed for MEDLINE]


16. Mov Disord. 1999 Jul;14(4):605-11.

Evolution of motor fluctuations in Parkinson's disease: a longitudinal study over
6 years.

Reardon KA, Shiff M, Kempster PA.

Department of Neurosciences, Monash Medical Centre, Clayton, Victoria, Australia.

A prospective longitudinal 6-year study of 34 patients with Parkinson's disease
from the time of initiation of drug treatment explored changes in the motor
response to L-dopa over the early to mid disease course. Motor fluctuations
developed in 41% after a mean L-dopa treatment interval of 25 months and
dyskinesia developed in 53% after a mean of 15 months' treatment. Patients who
developed fluctuations had a significantly better response to L-dopa than
nonfluctuators. Nonfluctuators also had significantly greater "midline" motor
disability affecting cranial and truncal muscles and gait. The development of
motor fluctuations may simply reflect a retained capacity to respond to L-dopa as
endogenous dopaminergic neurotransmission declines with progressive nigral cell
loss. Many patients who show no sign of motor fluctuation 5 or 6 years into the
disease course have a relatively blunted response to L-dopa. The proportion of
such cases seems to correspond to the percentage that have coexisting striatal
pathologic changes in postmortem studies.

PMID: 10435497 [PubMed - indexed for MEDLINE]


17. J Neurol Neurosurg Psychiatry. 1994 Nov;57(11):1444.

Motor response to apomorphine and levodopa in asymmetric Parkinson's disease.

Kempster PA, Lees AJ.

Comment on:
    J Neurol Neurosurg Psychiatry. 1994 May;57(5):562-6.

PMCID: 1073217
PMID: 7964840 [PubMed - indexed for MEDLINE]


18. J Neurol Neurosurg Psychiatry. 1994 Apr;57(4):430-4.

Motor response to levodopa in patients with parkinsonian motor fluctuations: a
follow-up study over three years.

Hughes AJ, Frankel JP, Kempster PA, Stern GM, Lees AJ.

Department of Neurology, University College and Middlesex Hospitals, School of
Medicine, London, UK.

To clarify the way in which the clinical response to levodopa changes with the
progression of Parkinson's disease, a longitudinal study was performed to
quantify motor response characteristics to single doses of levodopa by mouth over
three years in 23 patients with fluctuating motor function. A significant
increase in motor disability in "on" (time of peak motor improvement) and "off"
(before levodopa dose) phases occurred and "on" phase dyskinesia increased by
24%, though the amplitude of motor response was conserved. There was no evidence 
of progressive loss of response of certain motor deficits affecting axial muscles
and gait. The mean duration of motor response decreased by 17%. Both shortening
of response duration and increase in "off" phase disability contribute to the
development of motor fluctuations. A short response time to the levodopa test
dose was not an invariable finding in patients with severe fluctuations, whereas 
all had large response amplitudes and high "off" phase disability scores.
Patients who have developed motor fluctuations may continue to respond to
dopaminergic treatment until late in the disease course, despite the unstable
nature of their responses.

PMCID: 1072871
PMID: 8163991 [PubMed - indexed for MEDLINE]


19. Nutr Rev. 1994 Feb;52(2 Pt 1):51-8.

Dietary factors in the management of Parkinson's disease.

Kempster PA, Wahlqvist ML.

Department of Neurosciences, Monash Medical Centre, Melbourne, Australia.

Oral administration of L-dopa is currently the most effective way to treat the
cerebral dopamine deficiency which causes Parkinson's disease. Unfortunately,
many patients with advanced Parkinson's disease develop an unstable pattern of
response to L-dopa because of fluctuating delivery of the drug to the brain. Diet
contributes to this problem through its adverse effects on L-dopa
pharmacokinetics. This article reviews dietary strategies to improve
responsiveness to pharmaceutical L-dopa treatment and the potential use of food
as a source of L-dopa. Nutritional factors concerning weight loss and energy
balance in Parkinson's disease are also discussed. A set of dietary guidelines is
developed to assist clinical nutritionists and neurologists in the practical
management of patients with Parkinson's disease.

PMID: 8183469 [PubMed - indexed for MEDLINE]


20. Clin Exp Neurol. 1994;31:38-42.

Response to L-dopa and evolution of motor fluctuations in the early phase of
treatment of Parkinson's disease.

Shif M, Kempster PA.

Neurosciences Department, Monash Medical Centre, Clayton, Melbourne, Victoria.

Twenty patients with Parkinson's disease were studied during the early phase of
L-dopa treatment to clarify the development and progression of Parkinsonian motor
fluctuations. Two patients had developed symptomatic motor fluctuations of
moderate severity and another 3 had mild fluctuations. Both the initial response 
to L-dopa and the amplitude of response to a L-dopa test dose after a mean follow
up period of 30 months were significantly greater for the fluctuating patients
compared with those without fluctuation (p < 0.05). Although severe motor
fluctuations do not usually develop until a number of years of L-dopa treatment
have elapsed, this study shows that motor fluctuations can be detected quite
early in the disease course and tend to appear in those patients who respond best
to L-dopa.

PMID: 7586663 [PubMed - indexed for MEDLINE]

 

TITLE: Evolution of motor fluctuations in Parkinson's disease: a longitudinal study over 6 years.
AUTHORS: Reardon KA; Shiff M; Kempster PA
AUTHOR AFFILIATION: Department of Neurosciences, Monash Medical Centre, Clayton, Victoria, Australia.
SOURCE: Mov Disord 1999 Jul;14(4):605-11
CITATION IDS: PMID: 10435497 UI: 99361850
ABSTRACT: A prospective longitudinal 6-year study of 34 patients with Parkinson's disease from the time of initiation of drug treatment explored changes in the motor response to L-dopa over the early to mid disease course. Motor fluctuations developed in 41% after a mean L-dopa treatment interval of 25 months and dyskinesia developed in 53% after a mean of 15 months' treatment. Patients who developed fluctuations had a significantly better response to L-dopa than nonfluctuators. Nonfluctuators also had significantly greater "midline" motor disability affecting cranial and truncal muscles and gait. The development of motor fluctuations may simply reflect a retained capacity to respond to L-dopa as endogenous dopaminergic neurotransmission declines with progressive nigral cell loss. Many patients who show no sign of motor fluctuation 5 or 6 years into the disease course have a relatively blunted response to L-dopa. The proportion of such cases seems to correspond to the percentage that have coexisting striatal pathologic changes in postmortem studies.

1999/08
1999/06 10:00


--------------------------------------------------------------------------------


TITLE: Motor response to apomorphine and levodopa in asymmetric Parkinson's disease [letter; comment]
AUTHORS: Kempster PA; Lees AJ
SOURCE: J Neurol Neurosurg Psychiatry 1994 Nov;57(11):1444
CITATION IDS: PMID: 7964840 UI: 95054140
COMMENT: Comment on: J Neurol Neurosurg Psychiatry 1994 May;57(5):562-6
MAIN MESH HEADINGS: Apomorphine/*therapeutic use
Levodopa/*therapeutic use
Parkinson Disease/*drug therapy

1994/11
1994/01 00:00


--------------------------------------------------------------------------------


TITLE: Motor response to levodopa in patients with parkinsonian motor fluctuations: a follow-up study over three years.
AUTHORS: Hughes AJ; Frankel JP; Kempster PA; Stern GM; Lees AJ
AUTHOR AFFILIATION: Department of Neurology, University College and Middlesex Hospitals, School of Medicine, London, UK.
SOURCE: J Neurol Neurosurg Psychiatry 1994 Apr;57(4):430-4
CITATION IDS: PMID: 8163991 UI: 94216886
ABSTRACT: To clarify the way in which the clinical response to levodopa changes with the progression of Parkinson's disease, a longitudinal study was performed to quantify motor response characteristics to single doses of levodopa by mouth over three years in 23 patients with fluctuating motor function. A significant increase in motor disability in "on" (time of peak motor improvement) and "off" (before levodopa dose) phases occurred and "on" phase dyskinesia increased by 24%, though the amplitude of motor response was conserved. There was no evidence of progressive loss of response of certain motor deficits affecting axial muscles and gait. The mean duration of motor response decreased by 17%. Both shortening of response duration and increase in "off" phase disability contribute to the development of motor fluctuations. A short response time to the levodopa test dose was not an invariable finding in patients with severe fluctuations, whereas all had large response amplitudes and high "off" phase disability scores. Patients who have developed motor fluctuations may continue to respond to dopaminergic treatment until late in the disease course, despite the unstable nature of their responses.

1994/04
1994/01 00:00

--------------------------------------------------------------------------------


TITLE: Response to L-dopa and evolution of motor fluctuations in the early phase of treatment of Parkinson's disease.
AUTHORS: Shif M; Kempster PA
AUTHOR AFFILIATION: Neurosciences Department, Monash Medical Centre, Clayton, Melbourne, Victoria.
SOURCE: Clin Exp Neurol 1994;31:38-42
CITATION IDS: PMID: 7586663 UI: 96038313
ABSTRACT: Twenty patients with Parkinson's disease were studied during the early phase of L-dopa treatment to clarify the development and progression of Parkinsonian motor fluctuations. Two patients had developed symptomatic motor fluctuations of moderate severity and another 3 had mild fluctuations. Both the initial response to L-dopa and the amplitude of response to a L-dopa test dose after a mean follow up period of 30 months were significantly greater for the fluctuating patients compared with those without fluctuation (p < 0.05). Although severe motor fluctuations do not usually develop until a number of years of L-dopa treatment have elapsed, this study shows that motor fluctuations can be detected quite early in the disease course and tend to appear in those patients who respond best to L-dopa.

1994/01
1994/01 00:00

--------------------------------------------------------------------------------


TITLE: Intermittent subcutaneous apomorphine injection treatment for parkinsonian motor oscillations.
AUTHORS: Kempster PA; Iansek R; Larmour I
AUTHOR AFFILIATION: Monash Medical Centre, Melbourne, Vic., Australia.
SOURCE: Aust N Z J Med 1991 Jun;21(3):314-8
CITATION IDS: PMID: 1953509 UI: 92061778
ABSTRACT: Eight patients with severe Parkinsonian motor oscillations have been treated with the dopamine receptor agonist apomorphine by intermittent subcutaneous self-injection as an adjunct to oral anti-Parkinsonian medication. The dopamine receptor antagonist domperidone was also given by mouth to prevent nausea. Six patients remain on chronic treatment (mean period 6.5 months) with improved control of motor function in each case. Four have had major enhancement of their quality of life. Benefits of this treatment stem from the training of patients to use intelligent behaviour to administer a promptly acting and effective pharmacological agent, thereby exercising a degree of direct control over previously unpredictable variations in motor performance.

1991/06
1991/01 00:00

--------------------------------------------------------------------------------


TITLE: Diurnal differences in response to oral levodopa.
AUTHORS: Frankel JP; Pirtosek Z; Kempster PA; Bovingdon M; Webster R; Lees AJ; Stern GM
AUTHOR AFFILIATION: Department of Neurology, Middlesex and University College Hospitals School of Medicine, London.
SOURCE: J Neurol Neurosurg Psychiatry 1990 Nov;53(11):948-50
CITATION IDS: PMID: 2283524 UI: 91132227
ABSTRACT: Diurnal differences in duration and quality of motor response to levodopa are frequently described by patients. The quality and duration of motor responses were objectively assessed to morning and afternoon oral levodopa doses in five patients with Parkinsonian motor fluctuations who complained of diurnal variation in response to their normal levodopa medication. Results suggest that under controlled conditions which eliminated the effects of diet and overlapping levodopa effects the response to levodopa remained unchanged throughout the day, and that the duration of response could be predicted by plasma levodopa levels.

1990/11
1990/01 00:00


--------------------------------------------------------------------------------


TITLE: Comparison of motor response to apomorphine and levodopa in Parkinson's disease.
AUTHORS: Kempster PA; Frankel JP; Stern GM; Lees AJ
AUTHOR AFFILIATION: Department of Neurology, Middlesex and Hospital School of Medicine, University College, London.
SOURCE: J Neurol Neurosurg Psychiatry 1990 Nov;53(11):1004-7
CITATION IDS: PMID: 2283512 UI: 91132211
ABSTRACT: The magnitude and pattern of motor responses to single doses of subcutaneous apomorphine and oral levodopa were compared in 14 patients with Parkinson's disease. Although apomorphine produced much shorter motor responses than levodopa, the quality of response to the two drugs was virtually indistinguishable. These clinical observations support the notion that integrity of striatal post-synaptic dopamine receptors is a key determinant of responsiveness to dopaminergic treatment in Parkinson's disease.

1990/11
1990/01 00:00


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TITLE: Subcutaneous apomorphine in the treatment of Parkinson's disease.
AUTHORS: Frankel JP; Lees AJ; Kempster PA; Stern GM
AUTHOR AFFILIATION: Department of Neurology, Middlesex Hospital School of Medicine, London, United Kingdom.
SOURCE: J Neurol Neurosurg Psychiatry 1990 Feb;53(2):96-101
CITATION IDS: PMID: 2313313 UI: 90188437
ABSTRACT: Apomorphine a dopamine receptor agonist was given subcutaneously to 57 levodopa treated parkinsonian patients with refractory off-period disabilities for a median period of 16 months. In 30 given intermittent suprathreshold injections the mean number of hours spent in a disabling off state fell from 6.9 to 2.9. Similar benefit was observed in 21 patients receiving continuous infusions with additional boluses on demand by mini-pump (mean reduction of hours off from 9.9 to 4.5). Twelve patients have been treated for over two years without tachyphylaxis or loss of response. The incidence of neuropsychiatric side-effects has been low (7%). Six patients failed to show a sustained worthwhile response; severe disabilities during "on" periods being the major problem. Subcutaneous apomorphine is proposed as an effective treatment for patients with incapacitating "off" period disabilities refractory to oral medication and should be considered before experimental implantation procedures.

1990/02
1990/01 00:00


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