December 2013
Rob Wilson
Sunday 2 November 2014
Monday 18 August 2014
August 2013
August 2013
DEMENTIA
AGE RELATED
EARLY ONSET
ALZHEIMERS
Note: CBC News article Aug 22 , 10:25 PM –Cas Reusee- on
Mary Heckt who died at 81 and had significant signs of Vascular Dementia and
yet could still do drawing of faces from memory
- search for the interview with Dr Fornizari in Neurology
dept at U of T
Dementia
From Wikipedia, the free encyclopedia
Dementia (taken from Latin, originally meaning
"madness", from de- "without" + ment, the
root of mens "mind") is a serious loss of global cognitive ability in a previously
unimpaired person, beyond what might be expected from normal aging. It may be static, the
result of a unique global brain injury, or progressive,
resulting in long-term decline due to damage or disease in the body. Although
dementia is far more common in the geriatric population (about 5% of
those over 65 are said to be involved),[1]
it can occur before the age of 65, in which case it is termed "early onset
dementia".[2]
Dementia is not a single disease, but a
non-specific syndrome
(i.e., set of signs
and symptoms).
Affected cognitive areas can be memory, attention, language, and problem solving.
Normally, symptoms must be present for at least six months to support a
diagnosis.[3] Cognitive
dysfunction of shorter duration is called delirium.
Especially in later stages of the condition,
subjects may be disoriented
in time (not knowing the day, week, or even year), in place (not knowing where
they are), and in person (not knowing who they and/or others around them are).
Dementia can be classified as either reversible
or irreversible, depending upon the etiology of the disease. Fewer
than 10% of cases of dementia are due to causes that may be reversed with
treatment.
Some of the most common forms of dementia are: Alzheimer's disease,
vascular dementia,
frontotemporal dementia,
semantic dementia
and dementia with Lewy bodies.
Dementia is not merely a problem of memory. It
reduces the ability to learn, reason, retain or recall past experience and
there is also loss of patterns of thoughts, feelings and activities. Additional
mental and behavioral problems often affect people who have dementia, and may
influence quality of life, caregivers, and the need for institutionalization.
As dementia worsens individuals may neglect themselves and may become
disinhibited and may become incontinent. (Gelder et al. 2005). Behaviour
may be disorganized, restless or inappropriate. Some people become restless or
wander about by day and sometimes at night. When people with dementia are put
in circumstances beyond their abilities, there may be a sudden change to tears
or anger (a "catastrophic reaction").[4] A common symptom of dementia for dementia
sufferers to deny that relatives, even relatives in their immediate family, are
their own relatives.
Depression affects 20–30% of people who have
dementia, and about 20% have anxiety.[5]
Psychosis (often delusions of persecution) and agitation/aggression also often
accompany dementia. Each of these must be assessed and treated independently of
the underlying dementia.[6]
It is possible for a patient to exhibit two or
more dementing processes at the same time, as none of the known types of
dementia protects against the others. Indeed, about 10% of people with dementia
have what is known as mixed dementia, which may be a combination of
Alzheimer's disease and multi-infarct dementia.[7][8]
Various types of brain injury may cause
irreversible but fixed cognitive impairment. Traumatic brain injury
may cause generalized damage to the white matter of the brain (diffuse axonal injury),
or more localized damage (as also may neurosurgery). A temporary reduction
in the brain's supply of blood or oxygen may lead to hypoxic-ischemic injury.
Strokes
(ischemic stroke, or intracerebral, subarachnoid, subdural or extradural
hemorrhage) or infections (meningitis and/or encephalitis) affecting the brain,
prolonged epileptic seizures
and acute hydrocephalus
may also have long-term effects on cognition. Excessive alcohol use may cause alcohol dementia,
Wernicke's
encephalopathy and/or Korsakoff's psychosis.
Dementia that begins gradually and worsens
progressively over several years is usually caused by neurodegenerative
disease—that is, by conditions that affect only or
primarily the neurons of the brain and cause gradual but irreversible loss of
function of these cells. Less commonly, a non-degenerative condition may have
secondary effects on brain cells, which may or may not be reversible if the
condition is treated.
Causes of dementia depend on the age at which
symptoms begin. In the elderly population (usually defined in this context as
over 65 years of age), a large majority of dementia cases are caused by Alzheimer's disease,
vascular dementia,
or both. Dementia with Lewy
bodies is another commonly exhibited form, which
again may occur alongside either or both of the other causes.[9][10][11] Hypothyroidism sometimes causes slowly
progressive cognitive impairment as the main symptom, and this may be fully
reversible with treatment. Normal pressure
hydrocephalus, though relatively rare, is important to
recognize since treatment may prevent progression and improve other symptoms of
the condition. However, significant cognitive improvement is unusual.
Dementia is much less common under 65 years of
age. Alzheimer's disease is still the most frequent cause, but inherited forms
of the disease account for a higher proportion of cases in this age group. Frontotemporal lobar
degeneration and Huntington's disease
account for most of the remaining cases.[12] Vascular dementia
also occurs, but this in turn may be due to underlying conditions (including antiphospholipid
syndrome, CADASIL, MELAS, homocystinuria, moyamoya and Binswanger's disease).
People who receive frequent head trauma, such as boxers or football players,
are at risk of chronic traumatic
encephalopathy[13]
(also called dementia pugilistica
in boxers).
In young adults (up to 40 years of age) who
were previously of normal intelligence, it is very rare to develop dementia
without other features of neurological disease, or without features of disease
elsewhere in the body. Most cases of progressive cognitive disturbance in this
age group are caused by psychiatric illness, alcohol or other drugs, or
metabolic disturbance. However, certain genetic disorders can cause true
neurodegenerative dementia at this age. These include familial Alzheimer's
disease, SCA17
(dominant
inheritance); adrenoleukodystrophy
(X-linked);
Gaucher's disease
type 3, metachromatic
leukodystrophy, Niemann-Pick disease
type C, pantothenate
kinase-associated neurodegeneration, Tay-Sachs disease
and Wilson's disease
(all recessive).
Wilson's disease is particularly important since cognition can improve with
treatment.
At all ages, a substantial proportion of
patients who complain of memory difficulty or other cognitive symptoms have depression
rather than a neurodegenerative disease. Vitamin deficiencies and chronic
infections may also occur at any age; they usually cause other symptoms before
dementia occurs, but occasionally mimic degenerative dementia. These include
deficiencies of vitamin B12,
folate
or niacin,
and infective causes including cryptococcal meningitis,
HIV,
Lyme disease,
progressive multifocal
leukoencephalopathy, subacute sclerosing
panencephalitis, syphilis and Whipple's disease.
Creutzfeldt-Jakob
disease typically causes a dementia that worsens over
weeks to months, being caused by prions. The common causes of
slowly progressive dementia also sometimes present with rapid progression: Alzheimer's disease,
dementia with Lewy
bodies, frontotemporal lobar
degeneration (including corticobasal
degeneration and progressive
supranuclear palsy).
On the other hand, encephalopathy or delirium may develop relatively
slowly and resemble dementia. Possible causes include brain infection (viral encephalitis,
subacute sclerosing
panencephalitis, Whipple's disease)
or inflammation (limbic encephalitis,
Hashimoto's
encephalopathy, cerebral vasculitis);
tumors such as lymphoma
or glioma;
drug toxicity (e.g. anticonvulsant
drugs); metabolic causes such as liver failure
or kidney failure;
and chronic subdural hematoma.
There are many other medical and neurological
conditions in which dementia only occurs late in the illness. For example, a
proportion of patients with Parkinson's disease
develop dementia, though widely varying figures are quoted for this proportion.[citation needed] When dementia
occurs in Parkinson's disease, the underlying cause may be dementia with Lewy
bodies or Alzheimer's disease,
or both.[14] Cognitive impairment also occurs in
the Parkinson-plus syndromes of progressive
supranuclear palsy and corticobasal
degeneration (and the same underlying pathology may cause
the clinical syndromes of frontotemporal lobar
degeneration). Chronic inflammatory conditions of the brain
may affect cognition in the long term, including Behçet's disease,
multiple sclerosis,
sarcoidosis,
Sjögren's syndrome
and systemic lupus
erythematosus. Although the acute porphyrias may cause episodes of
confusion and psychiatric disturbance, dementia is a rare feature of these rare
diseases.
There are many specific types and causes of
dementia, often showing slightly different symptoms. However, the symptom
overlap is such that usually it is impossible to diagnose the type of dementia
by symptomatology alone. Diagnosis may be aided by brain scanning techniques. In some
cases certainty cannot be attained except with brain biopsy during life, or at autopsy in death. Proper
differential diagnosis between the types of dementia (cortical
and subcortical)
requires referral to a specialist.[citation needed]
Normally, symptoms must be present for at least
six months to support a diagnosis.[3]
Cognitive dysfunction of shorter duration is called delirium. Delirium can be easily
confused with dementia due to similar symptoms. Delirium is characterized by a
sudden onset, fluctuating course, a short duration (often lasting from hours to
weeks), and is primarily related to a somatic (or medical) disturbance. In
comparison, dementia has typically an insidious onset (except in the cases of a
stroke or trauma), slow decline of mental functioning, as well as a longer
duration (from months to years).[16]
Some mental illnesses,
including depression
and psychosis,
may produce symptoms that must be differentiated from both delirium and
dementia.[17]
Test
|
Sensitivity
|
Specificity
|
Reference
|
MMSE
|
71%–92%
|
56%–96%
|
[18]
|
3MS
|
83%–93.5%
|
85%–90%
|
[19]
|
AMTS
|
73%–100%
|
71%–100%
|
[19]
|
There exist some brief tests (5–15 minutes)
that have reasonable reliability to screen cognitive status. While many tests
have been studied,[20][21][22]
presently the mini mental state
examination (MMSE) is the best studied and most commonly
used, albeit some may emerge as better alternatives. Other examples include the
abbreviated mental test
score (AMTS), the, Modified Mini-Mental State Examination (3MS),[23] the Cognitive Abilities Screening
Instrument (CASI),[24]
the Trail-making test,[25] and the clock drawing test.[26]
Another approach to screening for dementia is
to ask an informant (relative or other supporter) to fill out a questionnaire
about the person's everyday cognitive functioning. Informant questionnaires
provide complementary information to brief cognitive tests. Probably the best
known questionnaire of this sort is the Informant Questionnaire
on Cognitive Decline in the Elderly (IQCODE).[27] On the other hand the General Practitioner
Assessment Of Cognition combines both, a patient assessment
and an informant interview. It was specifically designed for the use in the
primary care setting.
Clinical neuropsychologists provide diagnostic
consultation following administration of a full battery of cognitive testing,
often lasting several hours, to determine functional patterns of decline
associated with varying types of dementia. Tests of memory, executive function,
processing speed, attention, and language skills are relevant, as well as tests
of emotional and psychological adjustment. These tests assist with ruling out
other etiologies and determining relative cognitive decline over time or from
estimates of prior cognitive abilities.
Routine blood tests are also usually
performed to rule out treatable causes. These tests include vitamin B12, folic acid, thyroid-stimulating
hormone (TSH), C-reactive protein,
full blood count,
electrolytes,
calcium,
renal function,
and liver enzymes.
Abnormalities may suggest vitamin deficiency,
infection
or other problems that commonly cause confusion or disorientation in the
elderly. The problem is complicated by the fact that these cause confusion more
often in persons who have early dementia, so that "reversal" of such
problems may ultimately only be temporary.[citation needed]
Testing for alcohol and other known
dementia-inducing drugs may be indicated.
A CT scan
or magnetic resonance
imaging (MRI scan) is commonly performed, although
these modalities do not have optimal sensitivity for the diffuse metabolic
changes associated with dementia in a patient that shows no gross neurological
problems (such as paralysis or weakness) on neurological exam. CT or MRI may
suggest normal pressure
hydrocephalus, a potentially reversible cause of dementia,
and can yield information relevant to other types of dementia, such as
infarction (stroke)
that would point at a vascular type of dementia.
The functional neuroimaging
modalities of SPECT
and PET
are more useful in assessing long-standing cognitive dysfunction, since they
have shown similar ability to diagnose dementia as a clinical exam and
cognitive testing.[28]
The ability of SPECT to differentiate the vascular cause (i.e., multi-infarct dementia)
from Alzheimer's disease dementias, appears superior to differentiation by
clinical exam.[29]
Recent research has established the value of
PET imaging using carbon-11 Pittsburgh Compound B as a radiotracer (PIB-PET) in
predictive diagnosis of various kinds of dementia, in particular Alzheimer's disease.
Studies from Australia have found PIB-PET 86% accurate in predicting which
patients with mild cognitive impairment would develop Alzheimer's disease
within two years. In another study, carried out using 66 patients seen at the
University of Michigan, PET studies using either PIB or another radiotracer,
carbon-11 dihydrotetrabenazine (DTBZ), led to more accurate diagnosis for more
than one-fourth of patients with mild cognitive impairment or mild dementia.[30]
Many prevention measures have been proposed,
including both lifestyle changes and medication although none has been reliably
shown to be effective.
Except for the treatable types listed above,
there is no cure. Cholinesterase
inhibitors are often used early in the disease course.
Cognitive and behavioral interventions may also be appropriate. Educating and
providing emotional support to the caregiver (or carer) is of
importance as well elderly care.
Currently, no medications have been shown to
prevent or cure dementia.[31]
Medications are used to treat the behavioural and cognitive symptoms and have
no effect on the underlying pathophysiology.[32]
Acetylcholinesterase
inhibitors, such as donepezil, may be useful for
Alzheimer disease and other similar diseases causing dementia such as
Parkinsons or vascular dementia.[32]
The quality of the evidence however is poor.[33]
No difference has been shown between the agents in this family.[34] In a minority of people side effects including
bradycardia
and syncope.[35]
N-methyl-D-aspartate
(NMDA) receptor blockers such as memantine may be of benefit but
the evidence is less conclusive than for AChEIs.[36]
Due to their differing mechanisms of action memantine and acetylcholinesterase
inhibitors can be used in combination however the benefit is slight.[37][38]
Antidepressant
drugs: Depression
is frequently associated with dementia and generally worsens the degree of cognitive and behavioral impairment. Antidepressants effectively treat
the cognitive and behavioral symptoms of depression in patients with
Alzheimer's disease,[39]
but evidence for their use in other forms of dementia is weak.[40]
It is recommended that benzodiazepines
such as diazepam
be avoided in dementia due to the risks of increased cognitive impairment and
falls.[41] There is little evidence for the
effectiveness in this population.[42]
Antipsychotic drugs,
both typical antipsychotics
and atypical antipsychotics,
increase the risk of death in dementia.[43]
The use for dementia-associated behavior problems thus should only be
considered after other treatment modalities have failed and if the person in
question is at either risk to themselves or others.[41]
There is no solid evidence that folate or vitamin B12 improves outcomes in
those with cognitive problems.[44]
As people age, they experience more health
problems, and most health problems associated with aging carry a substantial
burden of pain; so, between 25% and 50% of older adults experience persistent
pain. Seniors with dementia experience the same prevalence of conditions likely
to cause pain as seniors without dementia.[45]
Pain is often overlooked in older adults and, when screened for, often poorly
assessed, especially among those with dementia since they become incapable of
informing others that they're in pain.[45][46]
Beyond the issue of humane care, unrelieved pain has functional implications.
Persistent pain can lead to decreased ambulation, depressed mood, sleep
disturbances, impaired appetite and exacerbation of cognitive impairment,[46] and pain-related interference with activity is
a factor contributing to falls in the elderly.[45][47]
Although persistent pain in the person with
dementia is difficult to communicate, diagnose and treat, failure to address
persistent pain has profound functional, psychosocial and quality of life
implications for this vulnerable population. Health professionals often lack
the skills and usually lack the time needed to recognize, accurately assess and
adequately monitor pain in people with dementia.[45][48]
Family members and friends can make a valuable contribution to the care of a
person with dementia by learning to recognize and assess their pain.
Educational resources (such as the Understand Pain and Dementia
tutorial) and observational assessment tools are available.[45][49][50]
In advanced dementia, people may lose the
ability to swallow effectively, leading to the consideration of gastrostomy feeding tube placement as a way to
give nutrition. Benefits of this procedure in those with advanced dementia has
not been shown.[51]
The risks include agitation, the person pulling out the tube, and tubes
becoming dislodged, clogged, or malpositioned among others. There is about a 1%
fatality rate directly related to the procedure[52]
with a 3% major complication rate.[53]
Adult daycare
centers as well as special care units in nursing homes often provide
specialized care for dementia patients. Adult daycare centers offer
supervision, recreation, meals, and limited health care to participants, as
well as providing respite for caregivers. In addition, home care can provide one-on-one
support and care in the home allowing for more individualized attention that is
needed as the disease progresses. Psychiatric nurses can make a distinctive contribution
to people's mentalness.[54]
Since dementia impairs normal communication due
to changes in receptive and expressive language, as well as the ability to plan
and problem solve, agitated behaviour is often a form of communication for the
person with dementia and actively searching for a potential cause, such as
pain, physical illness, or overstimulation can be helpful in reducing
agitation.[55]
Additionally, using an "ABC analysis of behaviour" can be a useful
tool for understanding behavior in people with dementia. It involves looking at
the antecedants (A), behavior (B), and consequences (C) associated with an
event to help define the problem and prevent further incidents that may arise
if the person's needs are misunderstood.[56]
Many countries consider the care of people
living with dementia to be a national priority, and invest in resources and
education to better inform health and social service workers, unpaid carers,
relatives and members of the wider community. Several countries have national
plans or strategies.[57]
In these national plans, there is recognition that people can live well with
dementia for a number of years, as long as there is the right support and
timely access to a diagnosis. David Cameron has described dementia
as being a "national crisis", affecting 800,000 people in the United Kingdom.[58]
In the United States, Florida's Baker Act allows law-enforcement
authorities and the judiciary to force mental evaluation
for those suspected of having developed dementia or other mental incapacities.[citation needed] In the United Kingdom, as with all mental
disorders, where a person with dementia could potentially be a danger to
themselves or others, they can be detained under the Mental Health Act 1983
for the purposes of assessment, care and treatment. This is a last resort, and
usually avoided if the patient has family or friends who can ensure care.
Driving
with dementia could lead to severe injury or even death to self and others.
Doctors should advise appropriate testing on when to quit driving.[59] The United Kingdom DVLA (Driving & Vehicle
Licensing Agency) states that people with dementia who specifically have poor
short term memory, disorientation, lack of insight or judgment are almost
certainly not fit to drive—and in these instances, the DVLA must be informed so
said license can be revoked. They do however acknowledge low-severity cases and
those with an early diagnosis, and those drivers may be permitted to drive
pending medical reports.
There are many support networks available to
those who have a diagnosis of dementia, and their families and carers. There
are also charitable organisations which aim to raise awareness and campaign for
the rights of people living with dementia.
Disability-adjusted
life year for Alzheimer and other dementias per
100,000 inhabitants in 2002.
<100
100-120
120-140
140-160
160-180
180-200
|
200-220
220-240
240-260
260-280
280–300
>300
|
The number of cases of dementia worldwide in
2010 was estimated at 35.6 million.[60]
Rates increase significantly with age, with dementia affecting 5% of the
population older than 65 and 20–40% of those older than 85.[1] Around two thirds of individuals with dementia
live in low and middle income countries, where the sharpest increases in
numbers are predicted.[61]
Rates are slightly higher in women than men at ages 65 and greater.[1]
Until the end of the 19th century, dementia was
a much broader clinical concept. It included mental illness and any type of
psychosocial incapacity, including conditions that could be reversed.[62] Dementia at this time simply referred to
anyone who had lost the ability to reason, and was applied equally to psychosis
of mental illness, "organic" diseases like syphilis that destroy the brain,
and to the dementia associated with old age, which was attributed to
"hardening of the arteries."
Dementia in the elderly was called senile
dementia or senility, and viewed as a normal and somewhat inevitable
aspect of growing old, rather than as being caused by any specific diseases. At
the same time, in 1907, a specific organic dementing process of early onset,
called Alzheimer's disease,
had been described. This was associated with particular microscopic changes in
the brain, but was seen as a rare disease of middle age.
Much like other diseases associated with aging,
dementia was rare before the 20th century, although by no means unknown, due to
the fact that it is most prevalent in people over 80, and such lifespans were
uncommon in preindustrial times. Conversely, syphilitic dementia was widespread
in the developed world until largely being eradicated by the use of penicillin
after WWII.
By the period of 1913–20, schizophrenia had been well-defined in
a way similar to today, and also the term dementia praecox
had been used to suggest the development of senile-type dementia at a younger
age. Eventually the two terms fused, so that until 1952 physicians used the
terms dementia praecox
(precocious dementia) and schizophrenia
interchangeably. The term precocious dementia for a mental illness
suggested that a type of mental illness like schizophrenia (including paranoia
and decreased cognitive capacity) could be expected to arrive normally in all
persons with greater age (see paraphrenia). After about 1920, the
beginning use of dementia for what we now understand as schizophrenia
and senile dementia helped limit the word's meaning to "permanent,
irreversible mental deterioration." This began the change to the more
recognizable use of the term today.
In 1976, neurologist Robert Katzmann suggested
a link between senile dementia and Alzheimer's disease.[63] Katzmann suggested that much of the senile
dementia occurring (by definition) after the age of 65, was pathologically
identical with Alzheimer's disease occurring before age 65 and therefore should
not be treated differently. He noted that the fact that "senile
dementia" was not considered a disease, but rather part of aging, was
keeping millions of aged patients experiencing what otherwise was identical
with Alzheimer's disease from being diagnosed as having a disease process,
rather than simply considered as aging normally.[64]
Katzmann thus suggested that Alzheimer's disease, if taken to occur over age
65, is actually common, not rare, and was the 4th or 5th leading cause of
death, even though rarely reported on death certificates in 1976.
This suggestion opened the view that dementia
is never normal, and must always be the result of a particular disease process,
and is not part of the normal healthy aging process, per se. The ensuing
debate led for a time to the proposed disease diagnosis of "senile
dementia of the Alzheimer's type" (SDAT) in persons over the age of 65,
with "Alzheimer's disease" diagnosed in persons younger than 65 who
had the same pathology. Eventually, however, it was agreed that the age limit
was artificial, and that Alzheimer's disease was the appropriate term for
persons with the particular brain pathology seen in this disease, regardless of
the age of the person with the diagnosis. A helpful finding was that although
the incidence of Alzheimer's disease increased with age (from 5–10% of
75-year-olds to as many as 40–50% of 90-year-olds), there was no age at which
all persons developed it, so it was not an inevitable consequence of aging, no
matter how great an age a person attained. Evidence of this is shown by
numerous documented supercentenarians (people living to 110+) that experienced
no serious cognitive impairment.
Also, after 1952, mental illnesses like
schizophrenia were removed from the category of organic brain syndromes,
and thus (by definition) removed from possible causes of "dementing
illnesses" (dementias). At the same, however, the traditional cause of
senile dementia– "hardening of the arteries" – now returned as a set
of dementias of vascular cause (small strokes). These were now termed multi-infarct
dementias or vascular dementias.
In the 21st century, a number of other types of
dementia have been differentiated from Alzheimer's disease and vascular
dementias (these two being the most common types). This differentiation is on
the basis of pathological examination of brain tissues, symptomatology, and by
different patterns of brain metabolic activity in nuclear medical imaging tests
such as SPECT
and PETscans
of the brain. The various forms of dementia have differing prognoses (expected
outcome of illness), and also differing sets of epidemologic risk factors. The
causal etiology of many of them, including Alzheimer's disease, remains
unknown, although many theories exist such as accumulation of protein plaques
as part of normal aging, inflammation, inadequate blood sugar, and traumatic
brain injury.
1.
^ a b c Sadock, Benjamin
James Sadock, Virginia Alcott (2008). Kaplan & Sadock's concise
textbook of clinical psychiatry (3rd ed.). Philadelphia: Wolters
Kluwer/Lippincott Williams & Wilkins. p. 52. ISBN 978-0-7817-8746-8.
2.
^ Fadil, H.,
Borazanci, A., Haddou, E. A. B.,Yahyaoui, M., Korniychuk, E., Jaffe, S. L.,
Minagar, A. (2009). "Early Onset Dementia". International Review
of Neurobiology. International Review of Neurobiology 84: 245–262. doi:10.1016/S0074-7742(09)00413-9. ISBN 978-0-12-374833-1. PMID 19501722.
4.
^ Geddes, John;
Gelder, Michael G.; Mayou, Richard (2005). Psychiatry. Oxford
[Oxfordshire]: Oxford University Press. p. 141. ISBN 0-19-852863-9. OCLC 56348037.
5.
^ Calleo J, Stanley
M (2008). "Anxiety Disorders in Later Life
Differentiated Diagnosis and Treatment Strategies". Psychiatric
Times 25 (8).
6.
^ Shub, Denis;
Kunik, Mark E (April 16, 2009). "Psychiatric Comorbidity in
Persons With Dementia: Assessment and Treatment Strategies". Psychiatric
Times 26 (4).
8.
^ Lee AY (2011). "Vascular dementia". Chonnam Med J
47 (2): 66–71. doi:10.4068/cmj.2011.47.2.66. PMC 3214877. PMID 22111063.
9.
^ Neuropathology
Group. Medical Research Council Cognitive Function and Aging Study (2001).
"Pathological correlates of late-onset dementia in a multicentre,
community-based population in England and Wales. Neuropathology Group of the
Medical Research Council Cognitive Function and Ageing Study (MRC CFAS)". Lancet
357 (9251): 169–75. doi:10.1016/S0140-6736(00)03589-3. PMID 11213093.
10.
^ Wakisaka Y et al.
(2003). "Age-associated prevalence and risk factors of Lewy body pathology
in a general population: the Hisayama study". Acta Neuropathol 106
(4): 374–82. doi:10.1007/s00401-003-0750-x. PMID 12904992.
11.
^ White L et al.
(2002). "Cerebrovascular pathology and dementia in autopsied Honolulu-Asia
Aging Study participants". Ann N Y Acad Sci 977 (9): 9–23. doi:10.1111/j.1749-6632.2002.tb04794.x. PMID 12480729.
12.
^ Ratnavalli E et
al. (2002). "The prevalence of frontotemporal dementia". Neurology
58 (11): 1615–21. doi:10.1212/WNL.58.11.1615. PMID 12058088.
13.
^ McKee A et al.
(2009). "Chronic Traumatic
Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head
Injury". J Neuropathol Exp Neurol 68 (7): 709–735. doi:10.1097/NEN.0b013e3181a9d503. PMC 2945234. PMID 19535999.
14.
^ Galvin JE et al.
(2006). "Clinical phenotype of Parkinson disease dementia". Neurology
67 (9): 1605–11. doi:10.1212/01.wnl.0000242630.52203.8f. PMID 17101891.
15.
^ Lamont P (2004). "Cognitive Decline in a Young Adult with Pre-Existent
Developmental Delay – What the Adult Neurologist Needs to Know". Practical
Neurology 4 (2): 70–87. doi:10.1111/j.1474-7766.2004.02-206.x.
16.
^ Caplan, J.P.,
& Rabinowitz, T. (2010). "An approach to the patient with cognitive
impairment: Delirium and dementia". The Medical clinics of North
America 94 (6): 1103–16, ix. doi:10.1016/j.mcna.2010.08.004. PMID 20951272.
18.
^ Boustani, M;
Peterson, B; Hanson, L; Harris, R; & Lohr, K; U.S. Preventive Services Task
Force (3 June 2003). "Screening for dementia in
primary care: a summary of the evidence for the U.S. Preventive Services Task
Force". Ann Intern Med 138 (11): 927–37. doi:10.7326/0003-4819-138-11-200306030-00015. PMID 12779304.
19.
^ a b Cullen B, O'Neill B, Evans JJ, Coen RF, Lawlor BA (2007). "A review of screening tests for
cognitive impairment". Journal of Neurology, Neurosurgery, and
Psychiatry 78 (8): 790–9. doi:10.1136/jnnp.2006.095414. PMC 2117747. PMID 17178826.
20.
^ Sager MA, Hermann
BP, La Rue A, Woodard JL (2006). "Screening for dementia in
community-based memory clinics" (PDF). Wisconsin medical journal 105
(7): 25–9. PMID 17163083.
21.
^ Fleisher, A;
Sowell, B; Taylor, C; Gamst, A; Petersen, R; Thal, L; Alzheimer's Disease
Cooperative Study (2007). "Clinical predictors of progression to Alzheimer
disease in amnestic mild cognitive impairment". Neurology 68
(19): 1588–95. doi:10.1212/01.wnl.0000258542.58725.4c. PMID 17287448.
22.
^ Karlawish, J
& Clark, C (2003). "Diagnostic evaluation of elderly patients with mild
memory problems". Ann Intern Med 138 (5): 411–9. doi:10.7326/0003-4819-138-5-200303040-00011. PMID 12614094.
23.
^ Teng EL, Chui HC
(1987). "The Modified Mini-Mental State (3MS) examination". The
Journal of Clinical Psychiatry 48 (8): 314–8. PMID 3611032.
24.
^ Teng EL, Hasegawa
K, Homma A, et al. (1994). "The Cognitive Abilities Screening Instrument
(CASI): a practical test for cross-cultural epidemiological studies of
dementia". International Psychogeriatrics / IPA 6 (1):
45–58; discussion 62. doi:10.1017/S1041610294001602. PMID 8054493.
25.
^ Tombaugh, T.N.T.N
(2004). "Trail Making test A and B: Normative Data Stratified by Age and
Education". Archives of Clinical Neuropsychology 19 (2):
203–214. doi:10.1016/S0887-6177(03)00039-8. PMID 15010086.
26.
^ Royall, D;
Cordes, J.; Polk, M. (1998). "CLOX: an executive clock
drawing task". J Neurol Neurosurg Psychiatry 64 (5): 588–94. doi:10.1136/jnnp.64.5.588. PMC 2170069. PMID 9598672.
27.
^ Jorm AF (2004).
"The Informant Questionnaire on cognitive decline in the elderly (IQCODE):
a review". International Psychogeriatrics / IPA 16 (3):
275–93. doi:10.1017/S1041610204000390. PMID 15559753.
28.
^ Bonte, FJ; Harris
TS, Hynan LS, Bigio EH, White CL 3rd (2006). "Tc-99m HMPAO SPECT in the
differential diagnosis of the dementias with histopathologic
confirmation". Clinical Nuclear Medicine 31 (7): 376–8. doi:10.1097/01.rlu.0000222736.81365.63. PMID 16785801.
29.
^ Dougall, NJ;
Bruggink S, Ebmeier KP (2004). "Systematic review of the diagnostic
accuracy of 99mTc-HMPAO-SPECT in dementia". The American Journal of
Geriatric Psychiatry 12 (6): 554–70. doi:10.1176/appi.ajgp.12.6.554. PMID 15545324.
30.
^ Abella HA (June
16, 2009). "Report from SNM: PET imaging of
brain chemistry bolsters characterization of dementias". Diagnostic
Imaging.
31.
^ Rafii, M. S.
& Aisen, P. S. (2009). "Recent developments in Alzheimer's disease
therapeutics". BMC medicine 7: 1–4. doi:10.1186/1741-7015-7-7.
32.
^ a b Lleó A, Greenberg SM, Growdon JH (2006). "Current
pharmacotherapy for Alzheimer's disease". Annu. Rev. Med. 57:
513–33. doi:10.1146/annurev.med.57.121304.131442. PMID 16409164.
33.
^ Rodda, J; Morgan,
S; Walker, Z (2009 Oct). "Are cholinesterase inhibitors effective in the
management of the behavioral and psychological symptoms of dementia in
Alzheimer's disease? A systematic review of randomized, placebo-controlled
trials of donepezil, rivastigmine and galantamine.". International
psychogeriatrics / IPA 21 (5): 813–24. doi:10.1017/S1041610209990354. PMID 19538824.
34.
^ Birks, J (2006
Jan 25). "Cholinesterase inhibitors for Alzheimer's disease.". Cochrane
database of systematic reviews (Online) (1): CD005593. doi:10.1002/14651858.CD005593. PMID 16437532.
35.
^ Gill S. S.,
Anderson, G. M., Fischer, H.D., Li, P., Normand, S. T. & Rochon, P. A.
(2009). "Syncope and its consequences in patients with dementia receiving
cholinesterase inhibitors: A population-based cohort study". Archives
of Internal Medicine 169 (9): 867–873. doi:10.1001/archinternmed.2009.43. PMID 19433698.
36.
^ Bond, M; Rogers,
G; Peters, J; Anderson, R; Hoyle, M; Miners, A; Moxham, T; Davis, S; Thokala,
P; Wailoo, A; Jeffreys, M; Hyde, C (2012). "The effectiveness and
cost-effectiveness of donepezil, galantamine, rivastigmine and memantine for
the treatment of Alzheimer's disease (review of Technology Appraisal No. 111):
a systematic review and economic model.". Health technology assessment
(Winchester, England) 16 (21): 1–470. doi:10.3310/hta16210. PMID 22541366.
37.
^ Raina P,
Santaguida P, Ismaila A, et al. (2008). "Effectiveness of cholinesterase inhibitors and
memantine for treating dementia: evidence review for a clinical practice
guideline". Annals of Internal Medicine 148 (5): 379–97. doi:10.7326/0003-4819-148-5-200803040-00009. PMID 18316756.
38.
^ Atri A,
Shaughnessy LW, Locascio JJ, Growdon JH (2008). "Long-term Course and
Effectiveness of Combination Therapy in Alzheimer's Disease". Alzheimer
Disease and Associated Disorders 22 (3): 209–21. doi:10.1097/WAD.0b013e31816653bc. PMC 2718545. PMID 18580597.
39.
^ Thompson S,
Herrmann N, Rapoport MJ, Lanctôt KL (2007). "Efficacy and safety of
antidepressants for treatment of depression in Alzheimer's disease: a
metaanalysis" (PDF). Canadian Journal of Psychiatry 52 (4): 248–55.
PMID 17500306.
40.
^ Bains J, Birks
JS, Dening TR (2002). "The efficacy of antidepressants in the treatment of
depression in dementia". In Dening, Tom. Cochrane Database of
Systematic Reviews (4): CD003944. doi:10.1002/14651858.CD003944. PMID 12519625.
41.
^ a b American Geriatrics Society 2012 Beers Criteria Update Expert,
Panel (2012 Apr). "American Geriatrics Society updated Beers Criteria for
potentially inappropriate medication use in older adults.". Journal of
the American Geriatrics Society 60 (4): 616–31. doi:10.1111/j.1532-5415.2012.03923.x. PMID 22376048.
42.
^ Lolk A, Gulmann
NC (2006). "[Psychopharmacological treatment of behavioral and
psychological symptoms in dementia]". Ugeskr Laeg (in Danish) 168
(40): 3429–32. PMID 17032610.
44.
^ Malouf, R;
Grimley Evans, J (2008 Oct 8). "Folic acid with or without vitamin B12 for
the prevention and treatment of healthy elderly and demented people". Cochrane
database of systematic reviews (Online) (4): CD004514. doi:10.1002/14651858.CD004514.pub2. PMID 18843658.
45.
^ a b c d e
Hadjistavropoulos, T et al.; Herr, K; Turk, DC; Fine, PG; Dworkin, RH; Helme,
R; Jackson, K; Parmelee, PA et al. (2007). "An interdisciplinary expert
consensus statement on assessment of pain in older persons". Clinical
Journal of Pain 23 (1 suppl): S1–43. doi:10.1097/AJP.0b013e31802be869. PMID 17179836.
46.
^ a b Shega, J; Emanuel, L; Vargish, L; Levine, S.K.; Bursch, H; Herr, K;
Karp, J.F.; Weiner, D.K. (2007). "Pain in persons with dementia: complex,
common, and challenging". Journal of Pain 8 (5): 373–8. doi:10.1016/j.jpain.2007.03.003. PMID 17485039.
47.
^ Blyth, F;
Cumming, M.R.; Mitchell, P; Wang, J.J. (2007). "Pain and falls in older
people". European Journal of Pain 11 (5): 564–71. doi:10.1016/j.ejpain.2006.08.001. PMID 17015026.
48.
^ Brown, C. (2009).
"Pain, aging and dementia: The
crisis is looming, but are we ready?". British Journal of Occupational
Therapy 72 (8): 371–75.
49.
^ Herr, K; Bjoro,
K; Decker, S; Wang (2006). "Tools for assessment of pain in nonverbal older
adults with dementia: a state-of-the-science review". Journal of
pain and symptom management 31 (2): 170–92. doi:10.1016/j.jpainsymman.2005.07.001. PMID 16488350.
50.
^ Stolee, P;
Hillier, LM; Esbaugh, et al.; Bol, N; McKellar, L; Gauthier, N (2005).
"Instruments for the assessment of pain in older persons with cognitive
impairment". Journal of the American geriatrics society 53
(2): 319–26. doi:10.1111/j.1532-5415.2005.53121.x. PMID 15673359.
51.
^ Sampson, EL;
Candy, B; Jones, L (2009 Apr 15). "Enteral tube feeding for older people
with advanced dementia.". Cochrane database of systematic reviews
(Online) (2): CD007209. doi:10.1002/14651858.CD007209.pub2. PMID 19370678.
52.
^ Lockett MA,
Templeton ML, Byrne TK, Norcross ED (2002). "Percutaneous endoscopic gastrostomy
complications in a tertiary-care center". Am Surg 68 (2):
117–20. PMID 11842953.
53.
^ Finocchiaro C,
Galletti R, Rovera G, et al. (1997). "Percutaneous endoscopic
gastrostomy: a long-term follow-up". Nutrition 13 (6):
520–3. doi:10.1016/S0899-9007(97)00030-0. PMID 9263232.
54.
^ Barker, Philip
(2003). Psychiatric and mental health nursing: the craft of caring.
London: Arnold. ISBN 0-340-81026-2. OCLC 53373798.
55.
^ Weitzel, T;
Robinson, S; Barnes, MR; Berry, TA; Holmes, JM; Mercer, S; Foster, T; Allen, L
et al. (2011). "The special needs of the hospitalized patient with
dementia". Medsurg nursing 20 (1): 13–8; quiz 19. PMID 21446290.
56.
^ Cunningham, C
(2006). "Understanding challenging behaviour in patients with
dementia". Nursing standard 20 (47): 42–5. PMID 16913375.
57.
^ "National Alzheimer and Dementia
Plans Planned Policies and Activities (PDF)". London: Alzheimer's Disease International. April 2012.
58.
^ Boseley, Sarah
(26 March 2012). "Dementia research funding to
more than double to £66m by 2015". The Guardian (London). ISSN 0261-3077. OCLC 60623878. Retrieved 27 April 2012.
60.
^ Alzheimer's
Disease International (2009). World Alzheimer Report 2009. p. 38.
Retrieved 11 March 2012.
61.
^ Alzheimer's
Disease International (2009). World Alzheimer Report 2009. p. 36.
Retrieved 11 March 2012.
62.
^ Berrios GE
(1987). "Dementia during the seventeenth and eighteenth centuries: a
conceptual history". Psychological Medicine 17 (4): 829–37. doi:10.1017/S0033291700000623. PMID 3324141.
63.
^ Kolata, Gina (June 17, 2010). "Drug Trials Test Bold Plan to
Slow Alzheimer's". The New York Times. Retrieved June 17, 2010.
64.
^ Katzman, R.
(1976). "The Prevalence and Malignancy of Alzheimer Disease: A Major
Killer". Archives of Neurology 33 (4): 217–218. doi:10.1001/archneur.1976.00500040001001. PMID 1259639.
Subscribe to:
Posts (Atom)