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dementia (updated 2002)

By Anne Wright,2014-05-08 21:35
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dementia (updated 2002)

    DEMENTIAS

    Notes Compiled by Kira Armstrong 9/15/02

    Term has been used since 1800’s

Characteristics

    1. Loss of function in multiple cognitive abilities

    2. (According to DSM diagnosis) Does NOT imply specific underlying cause, progressive course, OR

    irreversibility (it can be static, progressive or remitting)

    3. Distinction b/t delirium and dementia can be difficult (frequently may coexist)

    Some definitions do require persistence in order to exclude acute traumatic, metabolic, or toxic disorders

    DSM-IV Diagnosis requires memory impairment AND at least one kind of cognitive deficit (e.g., aphasia, apraxia, agnosia, executive function) ~ thereby distinguishing it from simple amnesia or aphasia Deficit must cause problems in occupational or social functioning

     Must be a decline from higher level of functioning

     Not occur exclusively during delirium

     DAT dx adds:

     Course is characterized by gradual onset and continuing cognitive decline

     Disturbance not better accounted for by another Axis I or medical disorder Disads of DSM definition

     Excludes patients with persevered memory (e.g. Pick‟s)

     Requirement for social/occupational disability renders definition imprecise

Onset

     Depends on etiology but generally happens late in life

     Uncommon in children but may occur as a result of a general medical condition

Prevalence

     approximately 5% of individuals >65 are severely demented and 10-15% are mildly impaired prevalence increases with age ; 20% or more of population are demented by age 85

     presenile dementia when re-examined 1-15 years later 25-57% failed to deteriorate in expected manner;

    believed due to unrecognized depression

     Alzheimer‟s most common, followed by vascular dementia (many patients have both)

Evaluation

     detailed history assess for inherited types of dementia

     evaluate for depression, hysteria, or psychosis

     explore medical history for strokes, seizures, TBI, alcohol/drug abuse, AIDS, endocrine dysfunction, vitamin

    deficiency (B12) and cancer

     Neurological exam and comprehensive evaluation of cognitive skills

    Cortical Dementias

    1. Alzheimer’s Disease

    (Dementia of the Alzheimer’s Type - DAT)

    loss of cholinergic neurons in the nucleus basalis of Meynert leading to development of senile plaques and neurofibrillary tangles

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    Dementia

    ~ 1~

characterized by marked deficits in memory, language and perception. Can also have symptoms of depression

    (quite common)

     onset between 40 and 90 years and becomes increasingly common w/advancing age; most commonly seen

    after age 65

     affects 5-10% of people over 65

     risk factors female, family history of down syndrome, TBI and history of thyroid disease

     diagnosis - typically a matter of exclusion; w/c makes it a catch all for all unrecognized dementias and renders

    DAT a nonspecific diagnosis; definitive dx can only made on autopsy

Neuropathologic features

    The primary motor, somatosensory, visual, and auditory cortices are relatively spared See Figure 19.14 on page 873 for a visual depiction.

    The following areas are generally affected first (and later, more severely). Listed in decreasing order: 1) medial temporal lobes, including amygdala, hippocampal formation, and entorhinal cortex

    2) basal temporal cortex extending over the lateral posterior temporal cortex, parieto-occipital cortex, and

    posterior cingulate gyrus

    3) frontal lobes

Changes include:

     Cerebral Atrophy

     Neuronal Loss prominent in the nucleus basalis, septal nuclei, and nucleus of the diagonal band where

    cholinergic projections arise. Also present to a lesser extent in locus ceruleus (norepinephrine) and raphe

    nuclei (serotonin).

     Amyloid Plaques (aka senile plaques) insoluble protein core containing beta-amyloid and apolipoprotein E

    (APOE) surrounded by abnormal axons and dendrites called dystrophic neuritis.

     Neurofibrillary Tangles intracellular accumulations of tau proteins prominent in the nucleus basalis,

    septal nuclei, and nucleus of the diagonal band where cholinergic projections arise. Also present to a lesser

    extent in locus ceruleus (norepinephrine) and raphe nuclei (serotonin).

Features

     Show more problems with short term memory and explicit vs. Implicit learning

     Remote memory relatively preserved, but may deteriorate in later stages

     associated w/anterograde memory loss, followed by retrograde; the first area of the brain to show pathology is

    the medial temporal cortex. As other areas b/c involved, (lateral temporal and frontal lobes) retrograde

    amnesia is observed

     Dominant early feature is memory loss (i.e., of recent memories or new learning). Next common feature is

    word-finding difficulty (i.e., anomic aphasia), along with apraxia and visuospatial deficits. Behavioral

    difficulties typically occur later in the disease course as compared to frontotemporal dementias, and

    hallucination are uncommon, especially early in the disease course unlike dementia with lewy bodies. Motor

    disturbances are usually not present early on; other diagnoses should be considered if motor disturbances are

    among the early clinical signs.

Three Primary Indications of Alzheimer’s:

    1. Neuritic Plaques - found chiefly in the cerebral cortex; these plaques are nonspecific they can be found in

    patients with Down‟s syndrome or other forms of dementia (can also be see in a diminished number in non-

    Alz. patients)

    2. Paired Helical filaments/neurofibrillary tangles - found in the cortex and the hippocampus (again, these are

    nonspecific) there is some debate in the literature re: whether plaques or tangles are most closely related to

    cognitive deterioration, however, most recent findings suggest that the amount of tangles is directly correlated

    w/degree of cognitive deterioration

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    Dementia

    ~ 2~

    3. Granulovacular Bodies - outer membranes with small dense granules in the center - more common in Alz

    patients than in the general aged population; degeneration of cells, occurs especially in hippocampus

Other Neuroanatomical Correlates

    1. Neocortical changes cortical atrophy loses as much as 1/3 of its volume as the disease progresses. This

    atrophy is not uniform:

     primary sensory and motor areas are spared

     most extensive change to parietal tertiary areas, inf. temporal cortex and limbic cortex (i.e., primarily

    the mesial temporal, parietal, and frontal convexity regions)

     frontal lobes also affected but less than those listed above

    2. Limbic cortex changes - the most severe degenerative changes. The Entorhinal cortex shows the most cell

    loss; responsible for relaying information to and from the neocortex and hippocampus. So, damage here is

    equivalent to loss of the hippocampal formation.

    3. Cell changes - there is a dispute as to whether cell are actually lost or whether they simply shrink. The more

    widespread cause of cortical atrophy appears to be the loss of dendritic arborization. It should be pointed out

    that elderly w/o Alz. appear to increase their arborization, so this sign is not merely a development associated

    with aging.

    4. Neurotransmitter Changes - although many studies emphasize the reduction of Ach in Alz. patients, it should

    be noted that in fact there are marked reductions in many transmitter systems and the patterns of loss are

    uneven from patient to patient. But strongest association between dementia and cell degeneration occurs with

    dysfunction in cholinergic neurons (hence newest interventions which focus on enhancing cholinergic function

    such as Tacrine)

Genetics

     Chromosome 19 associated with late-onset AD (after age 60) encodes APOE and has several different

    alleles. Presence of the E2 allele reduces the risk of developing AD, while presence of the E4 allele increases

    the risk (risk is increased the most with presence of E4 allele and history of head injury with LOC) thought

    to play a role in modulating plaque formation and clearance

     Chromosome 12 associated with late-onset AD encodes alpha2-macroglobulin (a protein). Two alleles

    have been identified that increase susceptibility thought to play a role in amyloid deposition. rdth Chromosome 21 associated with early-onset AD (as early as the 3 and 4 decade) mutations of the

    amyloid precursor protein connection with Down‟s syndrome (extra chromosome 21) whose victims develop

    early pathologic and clinical features of AD after age 30.

     Chromosome 1 also associated with early-onset AD mutations of the presenilin 1 and presenilin 2 genes.

    3 STAGES

    (which tend to occur in an orderly and consistent manner)

    Stage 1 (first 1-3 years)

     Memory new learning defective, mildly impaired remote memory

     Visuospatial skills topographic disorientation, poor complex construction

     Language - empty speech with few substantive words and paucity of ideas, anomia

     Personality indifference, occasional irritability

     Motor systems normal, including speech articulation

     EEG normal

     MRI/CT - normal

Stage 2 (2-10 years)

     Memory recent and remote recall more severely impaired

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    Dementia

    ~ 3~

     Visuospatial skills poor constructions, spatial disorientation; patients cannot find way about or copy

    constructions

     Language fluent aphasia, impaired comprehension, but relatively preserved repetition Cognitive skills severely impaired

     Calculation acalculia

     Praxis ideomotor apraxia

     Personality indifference or irritability

     Motor system restlessness, pacing

     EEG slowing of background rhythm

     CT/MRI normal or ventricular dilation and sulcal enlargement

     PET/SPECT bilateral parietal and frontal hypometabolism/hypoperfusion

Stage 3 (8-12 years)

     Intellectual functions severely impaired

     Language - verbal output is reduced to echolalia, palilalia or mutism

     Motor limbs assume a rigid and flexed position

     Sphincter control urinary and fecal incontinence

     CT scan - diffuse cerebral atrophy w/ventricular dilation and sulcal enlargement

     PET/SPECT bilateral parietal and frontal hypometabolism/hypoperfusion

     EEG diffusely slow

     death often results from pneumonia or urinary tract infection w/sepsis

Possible Causes of Alz.

    1. Genetics - possible cause; there is an increased frequency in families who have a member with Alz., and a

    higher risk if family members have Down‟s syndrome (perhaps caused by a gene/group of genes)

    2. Trace Metals - early studies w/ animals have shown neurofibrillary degeneration similar to what is seen in Alz.

    when they were given aluminum salts. Also, Alz. patients have an increase of 10 - 30 times the normal

    concentration of aluminum in their brains. But, earlier studies of link to aluminum have not been confirmed 3. Immune Reactions - some believe that in old age the immune system loses its ability to recognize it‟s own

    body and, therefore, develops antibodies w/c attack the brain and cause neuronal degeneration 4. Slow Viruses - some believe that it is caused by a virus w/ takes years to develop. (Creutzfeldt-Jakob’s disease

    appears to be caused by slow viruses w/c can be passed onto other humans and animals). Attempts to localize

    viruses have been unsuccessful.

    2. Pick’s Disease

    Rare disorder consisting of atrophy of frontal and temporal lobes from unknown causes

like DAT, it is also a cortical dementia

     characterized by symptoms that are virtually indistinguishable clinically from Alz., but at autopsy the disease

    can be distinguished, b/c atrophy is confined to the frontal and temporal cortex, and the plaques and tangles

    characteristic of Alz. are not present

     but, there are some differences between Pick‟s and Alz.

     Pick‟s patients have less memory, calculation and visuospatial impairments but more extravagant

    personality alterations

     both diseases produce aphasia, but Pick‟s have a greater tendency to produce a stereotyped verbal

    output, repeating the same story or joke again and again

     Kluver-Bucy symptoms; hyper oral tendencies are characteristic

     Pick‟s patients are also likely to demonstrate changes in personality and social conduct (consistent

    with frontal lobe deficits)

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    Dementia

    ~ 4~

     Normal EEG late in course of illness can also help to differentiate from Alz pathologically- focal atrophy in the frontal and/or anterior temporal lobes

     histologically - inflated neurons and neurons containing highly argyrophilic Pick bodies neuronal loss and a fibrillary gliosis of the subcortical white matter

     EEG normal

     On autopsy neurofibrillary tangles and senile plaques are absent

     NO selective involvement of a selective transmitter has been found

    3. Diffuse Lewy Body Dementia

    There is some controversy regarding how this dementia may be distinguished from Pick’s and/or Alzheimer’s dementias….

Characterized by:

     Fluctuating arousal throughout the day which leads to differences in overall cognitive functioning Visual hallucination

     Labile affect

     Parkinsonian symptoms but symptoms of dementia more similar to DAT

     These patients are NOT responsive to l-dopa, and are overly responsive to DA blocking agents Early age of onset

     Lewy bodies are found in the cortex rather than confined to the basal ganglia as they are in Parkinson‟s

    patients

    4. Creutzfeldt-Jacob’s Disease

    caused by a rapidly progressive viral infection of the nervous system w/c usually leads to death w/in 6 months of onset

     the virus is an unconventional slow virus w/c differs from conventional viral agents in its failure to stimulate

    an inflammatory or immune response, its invisibility to electron microscopes and its unusual resistance to

    traditional physical and chemical disinfection

     has been related to sporadic, familial and transmitted causes

     leads to generalized cortical atrophy

     symptoms may affect fxn of the spinal cord, cerebellum, extrapyramidal system or cortex as the disease progresses, the virus spreads to involve the nervous system diffusely and the patients eventually

    die in a vegetative state

     myoclonus is a prominent clinical finding but may not appear until late in the course of the disease differs from Alz. and Pick‟s, b/c its course is very rapid, leading in just a few months to stupor, coma and

    death.

     memory loss is prominent from the outset, but deterioration can be measured nearly day to day at autopsy there is a generalized thinning of the cortex and generalized abnormalities in subcortical structures may affect spinal cord, cerebellum, extrapyramidal system or cortex

     rare disorder occurs in 1/1,000,000

     clinical triad dementia, involuntary movements (especially myoclonus) and periodic EEG bovine spongioform encephalopathy considered a new variant of CJD associated with mad cow disease

    and has an earlier age of onset

Other Prion Related Dementias:

     kuru

     fatal familial insomnia

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    Dementia

    ~ 5~

bovine spongioform encephalopathy

Other Dementias of the Frontal Lobes

     Progressive subcortical gliosis extensive frontotemporal atrophy (like Pick‟s) but no Pick‟s cells

     Long duration of Creutzfeldt Jacob Disease

     On autopsy 10-15% of suspected Alz. Patients end up having another variant of a degenerative dementia with

    frontal and anterior temporal lobe pathology

    General definition of frontal lobe dementia-- a degenerative condition characterized by changes in personality, breakdown in social conduct, loss of social awareness and emotional empathy, disinhibition (the major finding),

    impulsivity, unconcern, changes in eating conduct (hyperphagia) and stereotyped and perseverative behavior.

    EXTRAPYRAMIDAL SYNDROMES W/DEMENTIA

    e.g.’s Huntington’s, Parkinson’s, Wilson’s disease and progressive supranuclear palsy

dementia is present in ~ 60% of patients w/ Parkinson’s disease (and approximately 93% have some deficits

    on npsych testing

     pathologically Parkinson‟s disease is characterized by loss of dopamine-containing cells in the substantia

    nigra

     Huntington’s disease - dementia is a uniform part of the disease and may be the initial symptoms preceding

    the appearance of chorea or other abnormalities

     pathologically - cellular loss in the caudate and putamen and some atrophy of the thalamus

    1. Huntington’s Chorea

    a degenerative loss of neurons in basal ganglia, frontal cortex and corpus callosum due to a genetic abnormality ~ leads to progressive intellectual deterioration and abnormal movements

autosomal dominant (chromosome 4); rare degenerative disorder approximately 5/100,000

     associated with repeats of the trinucleotide CAG (the more repeats you have, the more severe the disorder) usually diagnosed in late 30‟s or 40‟s although has been seen as young as 4 years

     patients known to have Huntington‟s disease are impaired at a broad range of memory, perceptual, and various

    frontal lobes tests

     presentation can be quite variable with cognitive or affective symptoms seen first; however, patients with

    early onset (e.g., childhood) frequently demonstrate parkinsonian symptoms rather than chorea first people in the at-risk groups appear to perform poorly only on the frontal lobe tests, suggesting that these tests

    may be useful as predictors

Symptoms

     dementia (concentration/attention; executive abilities; memory storage and retrieval)

     has both cortical and subcortical features, but disorders which do not occur include apraxia, aphasias

    and agnosias (w/c do result from progressive cortical disorders)

     choreiform movements frequent, discrete, brisk movements; jerks of pelvis, trunk, limbs, accompanied by

    dystonic posturing of the extremities and trunk; face has intermittent frowns, grimaces and smirks

     first symptom - usually a reduction of activity and restriction of interest

     first movements usually appear w/in a year after onset of psychiatric symptoms. The involuntary

    movements are initially slight and consist of little more than continuos fidgeting -- but increase until

    incessant

     the movements never involve single muscles but include whole limbs or parts of a limb

     they are also irregular and follow no sense of pattern

     eventually the movements b/c controllable and affect the head, face, trunk, and limbs - impeding all

    voluntary movements including speech and swallowing

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    Dementia

    ~ 6~

slow voluntary movements

     impaired saccades

     gait abnormality

     psychiatric disturbances (in ~ 50%)

     subtle alterations in personality, memory & motor coordination often the first symptoms oculomotor disturbance

     small percentage have parkinsonian features

     language affected later in disease, but hard to test b/c of dysarthria in later stages in absence of positive family history it is important to rule out Wilson‟s disease

Anatomy

     at autopsy brains are shown to show shrinkage and thinning of the cerebral cortex and the basal ganglia (in

    particular, the caudate) is grossly atrophied

     MRI and CT scan often show caudate atrophy, especially in later stages atrophy of the caudate frequently

    correlates with severity of the dementia

     theory - neurotransmitters w/c normally inhibit the DA pathways (GABA and NE) die during the course of the

    disease creating a hyperactive DA system - w/c leads to the chorea

    2. Parkinson’s Disease

    due to the degeneration of the substantia nigra and to the loss DA w/c is produced by this nucleus; the substantia

    nigra is the source of DA for the basal ganglia (Parkinson’s patients show a decrease of brain DA of over 90%)

although it is a subcortical dementia, can see some cortical changes…

     Most common extrapyramidal disorder affects 1/100 over age 65

     Does not appear to be inherited

     Environmental toxins may play a role

Features

     Clinically diagnosable dementia occurs in approximately 20-60%

     Bradyphrenia or mental slowing may occur early and in a large percent of clients Memory problems

     Executive problems

     Attentional difficulties

     Visuospatial deficits

     No cortical disturbances like aphasia or apraxia (later stages may show naming problems Depression relatively common (~30%)

     Disorders of movement (see below)

    4 Major Symptoms (resting tremor*, cogwheel rigidity*, bradykinesia*, and disturbances of posture) each of these symptoms can affect different body parts in different combinations. * “classic triad of symptoms”

     these symptoms can be divided into:

     positive symptoms - actions w/c are not seen in normals

     negative symptoms - inability to engage in behaviors that normals can Positive Symptoms include:

    1) Tremor at rest - stop during voluntary movements or during sleep; tremors often have a “pill rolling” quality.

    Are frequently asymmetrical!!

    2) Muscular rigidity - increased muscle tone simultaneously in both extensors and flexors - muscles allow

    movement for a short distance and then resist movement again (cogwheel effect)

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    Dementia

    ~ 7~

    3) Involuntary movements - may include continual changes in posture, sometimes to relieve tremor or stiffness,

    but often for no apparent reason - sometimes referred to as akathesia

Negative Symptoms Include:

    1) Disorders of posture - inability to maintain or difficulty in maintaining a part of the body in normal position

    (e.g., head may droop)

    2) Disorders of righting - difficulty in standing from a sitting position

    3) Disorders of locomotion - difficulty initiating stepping and when they do they shuffle; often once they begin to

    walk they take faster and faster steps and end up running (festinating gait)

    4) Disturbances of Speech - difficulties in the physical production of sound

    5) Akinesia - poverty or slowness of movement; may manifest itself in blankness of facial expression, lack of

    blinking, etc.

    6) Aphagia - difficulty in chewing and swallowing

Anatomy and Treatment

     Neuronal loss in substantia nigra, associated with Lewy bodies leading to decrease in striatal dopamine

    concentration

     Neurochemical deficiencies: dopamine (especially), acetylcholine, serotonin and corticotrophin releasing

    features

     Medications can help with motor symptoms, but do not improve cognitive deficits in fact, in some patients

    medications can cause confusion

     Similarly, neurosurgery will selectively help only one major physical symptom

     Pallidotomy can help treat the dyskinesia

     Thallotomy helps with the tremor (“t” helps with “t”)

    3. Other Extrapyramidal Dementias

    (i.e., “Parkinson +” or “Multisystem” dementias)

    1. Progressive supranuclear palsy (PSP) in addition to parkinsonism symptoms, causes swallowing difficulties

    and supranuclear opthalmoplegia

     Also known as Steele-Richardson-Olszewski syndrome

     Due to degeneration of multiple structures including the superior colliculus, red nucleus, dentate nucleus,

    subthalamic nucleus and globus pallidus

     Gaze paresis loss of downward gaze, leads to frequent falls and „dirty tie‟ sign

     Axial rigidity trunk/neck rigidity producing erect or hypererect rather than stooped posture

     Bradykinesia

     Pseudobulbar palsy masked face, increased jaw and facial jerks, exaggerated palatal and pharyngeal

    reflexes, dysphagia, drooling, emotional lability

     Gait disorder, falls and akinesia can also be present

     “wide-eyed stare”

    2. Wilson’s disease characterized by hepatic and CNS dysfunction due to abnormalities in copper metabolism;

    peak onset teens-20‟s

     Neurologic symptoms include Parkinsonian symptoms such as tremor, rigidity, dysarthria, and akinesia,

    as well as dystonia, “wingbeating tremor,” and ataxia

     Psychosis, mood changes and dementia can also occur

     Treatable if diagnosed early

     Autosomal recessive disorder (chromosome 13)

     Kaiser Fleischer rings are present in most cases while it is pathognomonic it may not be seen in every

    patient

THE FINE PRINT: Caveat emptor! These study materials have helped many people who have successfully completed the ABCN board certification process, but there is no guarantee that they will work for you. The notes’ authors, web site host, and everyone else involved in the creation and distribution of these study notes make no promises as to the complete accuracy of the material, and invite you to suggest changes.

    Dementia

    ~ 8~

3. Hallerverorden-Spatz disease rare inherited and progressive illness with late childhood or early adolescent

    onset, characterized by dementia with spasticity and rigidity, dystonia or chorea. Caused by an accumulation of

    iron in the brain. There is no current cure.

    4. Syndenham’s Chorea affects children between the ages of 5 and 15

     Associated with rheumatic fever and Pandas

     Also frequently associated with tics, tourette‟s, ADHD and dystonia

    5. Subacute Sclerosing Panencephalitis (SSPE)

     Develops primarily in children

     Poor school work, behavioral disturbance, restlessness, personality change ---- dementia

     Myoclonus is a characteristic symptom

     Rarely develops in adults

     Measles may be a cause

6. Shy Drager Syndrome

     Parkinson‟s symptoms + autonomic disturbance (impotence, urinary incontinence)

7. Olivopontocerebellar atrophy

     Parkinson‟s symptoms + ataxia – but NO rigidity or bradykinesia (DOES have tremor)

8. Striato-Nigral Degeneration

     Patients become stiff and slow develop difficulty with walking and balance

     Usually do not have a tremor, but cannot be distinguished from PD patients by a neurological exam alone

     Do not respond to L-dopa

     Can be distinguished from PD on autopsy because most of the damage is in the striatum rather than the

    substantia nigra

    MULTI-INFARCT DEMENTIA

    specific characteristics are variable, but includes psychomotor retardation and emotional lability in most cases

Second most common form of dementia following Alzheimer‟s

History:

     abrupt onset

     stepwise deterioration/fluctuating course

     previous stroke or transient ischemic attacks

     previous hypertension or other cardiovascular disease

Neurological Examination

     focal deficits

     pseudobulbar palsy (w/ dysarthria)

     gait disturbance

     psychomotor retardation

Mental Status Exam

     dementia (cortical and/or subcortical features)

     depression

     emotional lability

     relative preservation of personality

THE FINE PRINT: Caveat emptor! These study materials have helped many people who have successfully completed the ABCN board certification process, but there is no guarantee that they will work for you. The notes’ authors, web site host, and everyone else involved in the creation and distribution of these study notes make no promises as to the complete accuracy of the material, and invite you to suggest changes.

    Dementia

    ~ 9~

Laboratory assessment

     focal slowing on EEG

     infarcts usually visible on CT (but normal scan does not preclude the diagnosis )

Treatment

     discovery and treatment of underlying risk factors (e.g., emboli, hypertension, smoking, diabetes) Dysarthria and aphasia may improve w/ speech and language therapy

Risk Factors

     Hypertension, abnormal lipid levels, smoking, diabetes, and obesity Patients with cerebrovascular disease may have vascular disease AND episodes of coronary insufficiency with

    associated systemic hypotension leading to more diffuse brain damage

Key factors to differentiate from DAT

     Abrupt onset

     Stepwise deterioration

     Focal neurological symptoms

     Risk factors for vascular disease

     Tend to have an earlier onset that DAT and are more common in men

Lacunar Strokes see vascular notes

    Binswanger’s disease – when strokes are limited to white matter double check notes have it both for gray and

    for white matter…

    Other Causes of Dementia

    1. Vasculitis Dementia

     Caused by inflammation of the cranial arteries

     Often associated with systemic illnesses such as giant cell arteritis and lupus

    2. Bacterial Infections Producing Dementia

     syphillic general paresis is probably the best known example. It is currently rare; typically appears 15

     30 years after the initial infection and is characterized by progressive intellectual impairment combined in

    some cases w/ psychosis

     manifests as multiple strokes and associated dementia

     also accompanied by changes in personality

     examination of CSF can lead to definitive dx

     Lyme disease symptoms include facial palsy, headaches, peripheral neuropathy, meningitis, memory

    difficulties, irritability, depressed mood

     African trypanosomiasis African sleeping sickness transmitted by the tsetse fly

    3. Viral Infections Producing Dementia

    Dementia can be caused by acute encephalitis or by affects of neurotransmitter dysfunction, demyelination, etc.

     Postinfection encephalomyelitis may be caused by measles, varicella, rubella and other viral illnesses HIV Type 1 encephalopathy (see it‟s own section below)

     Progressive multifocal leukoencephalopthy due to an opportunistic infection that occurs in

    immunologically compromised individuals

THE FINE PRINT: Caveat emptor! These study materials have helped many people who have successfully completed the ABCN board certification process, but there is no guarantee that they will work for you. The notes’ authors, web site host, and everyone else involved in the creation and distribution of these study notes make no promises as to the complete accuracy of the material, and invite you to suggest changes.

    Dementia

    ~ 10~

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