A most excellent job, janet, but you're depressing me...
                Only kidding,
                Carole
P.S. On the bright side, last time I looked, I wasn't
demented or psychotic. I personally find the prospect of
psychiatric disability much scarier than physical
disability. But we Parkies have it all, don't we?

--- janet paterson <[log in to unmask]> wrote:
> Depression, Psychosis, and Dementia in Parkinson's
> Disease,
> EPDA one day conference  London 23rd-26th March, 1997
>
> Professor Jenner, Professor of Pharmacology, King's
> College Hospital, London
>
> Between 30 and 50% of Parkinson's patients experience
> depression; 20 to 40% dementia; 5 to 10% psychosis; and
> 15 to 20% drug induced psychosis. Clinicians often fail
> to deal with the neurobehavioural consequences of the
> disease. Treatment with dopamine agonists does not
> improve symptoms and may exacerbate other aspects of the
> disease; SSRI drugs can help. Dopaminergic cells
> throughout the brain are lost in the course of
> Parkinson's disease and are replaced by Lewy bodies, but
> it is not known if these changes produce the
> characteristic depression of the disease. Similarly,
> noradrenaline is also reduced by up to 50% in the limbic
> system and brainstem of sufferers and by over 75% in the
> frontal cortex: again, it is not known whether this
> causes dementia in patients; 5 HT reduction is associated
> with depression and psychosis, but is it cause or effect?
> Vascular disease and Alzheimer's disease symptoms may
> also be present, complicating the picture. What
> constitutes true Parkinson's!
>  dis
> ease pathology?
>
> Professor Poewe, Department of Neurology, University
> Hospital, Innsbruck, Austria
>
> The prevalence of depression in Parkinson's disease
> averages about 40%, and may precede the appearance of
> motor symptoms in a third of patients, suggestive of the
> pre morbid personality theory of Parkinson's disease.
> There is no correlation between the degree of depression
> and severity of disease, but depression is a risk factor
> for cognitive decline and more rapid progression to
> disability. Treatment comprises psychosocial support;
> behavioural therapies; drugs: 'levodopa', dopamine
> agonists, 'deprenyl'; tricyclic antidepressants; 'SSRIs'
> and ECT or 'TMS'. The three step treatment comprises
> substitution of brain dopamine, followed by tricyclic
> antidepressants, and then an SSRI. Symptoms include: loss
> of interest and initiative; indecisiveness; guilt
> feelings; loss of self-esteem; suicidal thoughts (but
> rarely suicide itself, which distinguishes it from non
> Parkinson depression); poor concentration; anxiety and
> panic attacks; fatigue; disrupted sleep patterns.
>
> The areas of clinical overlap between motor symptoms,
> depression, and cognitive decline include reduced levels
> of: concentration and judgment; memory; psychomotor
> speed; cognitive processing speed; and higher levels of
> sleep disorders and mood swings. Patients often fail to
> discern voice tones and can no longer recognise humour.
>
> Professor Cote, Columbia Presbyterian Medical Center,
> Neurological Institute, New York, USA
>
> Depression may be present for many years before
> Parkinson's disease is diagnosed, but it is very
> difficult to recognise, because there are so many
> neurobehavioural changes in Parkinson's that could be
> mistaken for depression. The pre morbid personality
> traits include introversion, inflexibility, being a non
> drinker, having difficulty making sexual contacts, lack
> of competitive spirit, and inability to fantasise. An
> indicator of future disease in smokers may be giving up
> smoking some 5 to 15 years before diagnosis, because of
> the dependency of addictive drives on dopamine. The
> mental changes caused by Parkinson's disease include
> depression which often occurs early in the course of the
> disease. Treatment with tricyclics disguises Parkinson
> symptoms; SSRIs, on the other hand, can exacerbate
> symptoms. Depression may last from a few days to several
> weeks at a time. Symptoms of Parkinson's depression
> include: feelings of hopelessness/worthlessness; no
> interest in pleasure; guilt; su!
> icid
> al thoughts; fearfulness; reduced appetite; weight loss;
> disrupted sleep. Parkinson patients who are not depressed
> have significant reductions in serotonin metabolites, but
> in those who are depressed, the degree of reduction
> parallels the degree of depression. Treatment with
> levodopa can increase motor symptoms and provoke a
> withdrawal syndrome, which can itself generate depressive
> feelings. Low dose tricyclics with low levels of
> cholinergic action, SSRIs, ECT, psychotherapy, and light
> therapy are recommended.
>
> Dr Eric Wolters, Department of Neurology, Academic
> Hospital, Wrije Universiteit, Amsterdam, The Netherlands
>
> Degeneration of dopaminergic cells and their replacement
> by Lewy bodies in the brain tissue is a hallmark of
> Parkinson's disease. The process is diffuse, occurring in
> the brainstem, striatal, frontal, and limbic regions.
> Striatal changes produce motor symptoms, those in the
> frontal and limbic regions psychiatric symptoms,
> including dementia and psychosis. Drug treatments induce
> a range of psychiatric symptoms, as a result of their
> anticholinergic and dopaminergic actions.
> Neuropsychiatric side effects are seen in about 20% of
> non demented and in 80% of demented patients. Dose is
> thought to be an important factor. Delirium is more
> common in elderly patients because acetylcholine
> production reduces with age, especially in dementing
> illnesses. Efforts must be made to reduce sensory
> deprivation. Psychosis is characterised by delusions
> and/or hallucinations, which subsequently become
> extremely frightening. Mild neuroleptics or atypical
> neuroleptics are advised; dopamine agonists sh!
> ould
>  be discontinued. Carers need to be informed about the
> consequences of drug treatment in Parkinson's disease.
>
> Professor Melamed, Department of Neurology, Rabin Medical
> Center, Tel Aviv University, Sackler School of Medicine,
> Israel
>
> Psychosis is the major non motor problem in Parkinson's
> disease, because it is a significant marker of disease
> deterioration and progression, and it's the most limiting
> factor in the treatment of motor symptoms in advanced
> disease. This is because of the requirement for high
> doses of levodopa and other drugs, long term use of which
> produce psychiatric symptoms. Psychosis is also the most
> common cause of admission of Parkinson patients into
> nursing homes. It may develop or worsen after infection,
> physical injury, surgery, or mental stress, and tends to
> be more common in older and demented patients. Several
> mechanisms are probably involved in its development. It
> is characterised by hallucinations, which at first are
> often benign, but these gradually become more frightening
> and disabling, resulting in aggression and severe
> agitation. Treatment has traditionally been to reduce
> levodopa and other antiparkinson drugs and substitute
> neuroleptics. However, these can produce a rapid an!
> d so
> metimes life threatening deterioration in motor symptoms.
> Ondansetron, an anti emetic used in the treatment of
> cancer, is well tolerated, with minimal side effects, but
> it is very expensive, and needs to be given in high
> doses.
>
> Professor Oertel, Neurology Clinic, Centre for Nervous
> Diseases, Philipps University, Marburg, Germany
>
> Dementia is acquired global impairment of higher cortical
> function, with a decline in memory, abstract thinking,
> and visuo spatial processing. It is a 'syndrome', with
> between 15 and 30% of patients with Parkinson's disease
> affected. Dementia can be part of depression, or, result
> from vascular disease or concurrent Alzheimer's disease:
> up to 20% of demented patients have both. About 5% of
> Parkinson patients also have Alzheimer's disease. Young
> onset Parkinson patients (35-40) rarely become demented,
> even at 65 and older, and Parkinson's is not a risk
> factor for dementia. Depression and dementia are,
> however, significantly correlated with Parkinson's
> disease. Dementia occurs when the neurofibrillary tangles
> strangle the nuclei of nerve cells in the brain, and
> plaques develop in the cortical areas. It begins in the
> temporal lobe, with a lesion the size of a 50p coin, and
> spreads. Dopamine levels are reduced as are levels of
> acetylcholine, hallmarks of both Alzheimer's and Parkin!
> son'
> s disease, but although patients with Apo E deposits
> develop cognitive impairments earlier than those without,
> these deposits are only a risk factor for Alzheimer's
> disease. Symptoms include apraxia, aphasia, personality
> changes, compromised short term memory, confusion,
> hallucinations, bradyphrenia and depression. Treatment is
> limited and may exacerbate other Parkinson's symptoms.
> Behavioural and occupational therapies, and psychosocial
> support are vital for the patient and his/her family.
>
> Professor Ellgring, Institute for Psychology, University
> of Wuerzburg, Germany
>
> Depression, dementia, and psychosis stretch the emotional
> resources of the families and carers of Parkinson's
> patients. Demands for care and social interaction are
> increased; there are adverse effects on health; stress
> increases; social isolation may result; and there are
> financial implications. These are compounded when the
> carer is elderly. The major concerns for carers of
> patients with Parkinson's and Alzheimer's focus on
> worries about the future, fear of leaving the patient
> unattended, and being misunderstood by the family. Carers
> are conflicted over encouraging independence in the
> patient; having to assume all the responsibility;
> restrictions on their own lifestyle; and feeling
> impatient and angry. Mental health problems among carers
> are common, and often become worse when the patient is
> transferred to a nursing home because of the attendant
> guilt, loneliness, and loss of identity. Sleep disorders
> and somatic illness are also common. There are times when
> both patient and !
>
=== message truncated ===


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