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B21 DDx of Dementia
Terms in this set (79)
The term dementia refers to
acquired chronic or progressive deterioration in brain function resulting in deficits in mentation and impairment in intellectual, social, and occupational functioning
Domains for dementia
memory, executive function, language, visuospatial function, emotional expression and personality
Features of cortical dysfunction include
aphasia, visuospatial dysfunction, apraxia, and agnosia
ability to appreciate position of objects in space, integrate obj's into coherent spatial framework, perform cognitive and motor tasks involving spatial conceptions
Visuospatial dysfunction occurs with lesions or degen processes involving what areas
occipital, parietal, and/or temporal lobes
How might pts present who have visuospatial dysfunction?
difficulty dressing, grooming, using utensils, or tools, or negotiating their surroundings
How do you test visuospatial function?
copy a design (esp 3-D figure)
What does apraxia refer to?
loss of ability to carry out learned, skilled movements despite intact primary sensory and motor pathways (and absence of impaired language or comprehension as contributing factors)
What are the 2 types of apraxia?
ideomotor and ideational
inability to MIMIC a movement in repsonse to a verbal command, i.e. "if you had a toothrbush in your hand..."
inability to carry out motor activities that involve mutliple, sequential components; i.e. pick up a pen and write a sentence, or wash your hands
inability to identify objects, shapes, sounds, smells, or people despite having knowledge of their characteristics and intact primary sensory pwys
Features of subcortical dysfunction
slowing of cognition and responsiveness, inattention, lack of spontaneity, drive, or motivation (irritability, mood changes common too)
Cortical and subcortical dysfunction can result in problems with
What is executive funciton?
ability to process and interpret information, make judgements and decisions based on that info, and carry out appropriate response
Areas of brain most impt for executive functioning
prefrontal lobes and associated subcortical white matter pwys and nuclear groups, i.e. MEDIAL DORSAL nucleus of thalamus
Patients with executive dysfunction have difficulty
anticipating and adapting to changes, poor planning ability, and learning from their mistakes
What is the main alternative diagnosis of dimentia?
What is delirium?
ACUTE decline in attention and cognition with perceptual disturbances and fluctuations in conscoiusness, typically due to underlying med condition
What is the difference in attention btwn delirium and dementia?
delirium: impaired attn; dementia: attention maintained until late in dz
Mental status exam tests what 6 domains?
orientation, registration, attention, calculation, recall, language
What does the MMSE NOT adequately evaluate?
What is a more in-depth exam of cognitive function?
neuropsychological evaluation (NPE)
What is gait abnormality a sign for?
Parkinson-assoc dementa, vascular dementia, or normal pressure hydrocephalus
If patient is confused or has a headache, what must the physician always do?
Fundoscopic exam -- papilledema
Frontal release signs
group of primitive reflexes (motor responses present in normal early dvl and subsequently inhibited) -- released from inhibition by damage to frontal lobes or underlying white matter pwys
5 frontal release signs
grasp, palmomental, snout, rooting, glabellar
Paraneoplastic syndrome that produces dementia
paraneoplastic encephalitis or limbic encephalitis -- autoimmune process; usually from small cell lung cancer
Triad for normal pressure hydrocephalus
gait abnormality, urinary incontinence, cognitive dysfunction (Wacky, wobbly, wet)
What type of dementia (location in brain) in NPH?
subcortical type with inattention, slowness to respond, and lack of spontaneity
What is the gait abnormality in NPH?
magnetic gait, feet stuck to floor
Cause of normal pressure hydrocephalus?
increased CSF volume due ot increasd production and/or decreased absorption of CSF; may be primary, secondary, or due to subarachnoid hemorrhage, or meningitis
Evaluation of NPH
Imaging, then large volume LP=diagnostic AND therapeutic
What does Vitamin B12 deficiency cause?
subacute combined degeneration; macrocytic anemia, peripheral neuropahty, cognitive dysfunction
Deficiency in vitamin B1 can cause
Triad of Wernicke's encephalopathy
cognitive dysfunction, ataxia, oculomotor abnormalities (ophthalmoplegia or nystagmus)
Structural changes in Wernicke's encephalopahty
symmetrical damage to structures surrounding 3rd ventricle, cerebral aqueduct, and 4th ventricle -- periventric regions of thal, hypothal (mamillary bodies esp**) oculomotor nuclei, PAG, and cerebellar vermis
What can Wernicke's encephalopathy progress to? Symptoms?
Wernicke-Korsakoff syndrome; profound retrograde and anterograde amnesia, and to fill in memory gaps, patients CONFABULATE
Initial workup of dementia should include
complete metabolic profile, including liver function tests and thyroid studies
Young pt with liver dysfunction and cognitive changes might have
Wilson's dz; autosomal recessive disorder of copper metabolism,
Pts with Wilson's dz may develop what neuro symptoms? Why?
Movement disorders --> basal ganglia, especially lentiform nuclei, are targeted
patients with depression may manifest symptoms of dementia without an underlying pathological process other than depression
What symptom is the hallmark of Alzheimer's dz?
Memory deficit; presents early in the dz course
Imaging with CT or MRI shows
diffuse cortical atrophy with prominent sulci and compensatory ventricular dilation; parietal and temporal lobes (esp hippocampus) more involved than other areas
Mild Cognitive Impairment
memory difficulty, intermediate stage between cognitive changes of nml aging and AD
Second most common type of primary neurodegenerative dementia?
Dementia with Lewy Bodies (DLB)
Core features of DLB
progressive cognitive dysfunction, visual hallucinations, fluctuating levels of attention and alertness/arousal, extrapyramidal (parkinson's" signs i.e. rigidity, tremor, bradykinesia, gait difficulty
Other features of DLB
autonomic dysfunction, i.e. orthostatic hypotention, impotence, urinary incontinence, and constipation
Compared to AD, DLB have more difficulty with
executive function and visuospatial function early in the dz course; memory less affected initially
Key neuropathological feature of DLB is presence of lewy bodies in what areas of the brain?
cortex, amygdala, cingulate gyrus, and substantia nigra
Generally, what are Lewy bodies?
abnormal aggregates of protein inside nerve cells
"Types" of frontotemporal lobar degeneration
frontotemporal dementia, Pick's dz, primary progressive aphasias
What are the primary progressive aphasias?
progressive nonfluent aphasia, and semantic dementia
Frontotemporal dementia (FTD) key feature
decline in social conduct that precedes impairment in cognition
Later in the dz, FTD, what happens?
verbal output diminishes
When does FTD usually present?
earlier than AD, in 6th decade
Pathophysiology of frontotemporal dementia
abnormal tau proteins with neuronal loss and lgiosis; dense silver-staning intraneural inclusions called Pick bodies
FTD with pick bodies present
FTD on neuroimaging
atrophy of frontal or temporal lobes on one or both sides
After dx of FTD, how long until death?
Progressive nonfluent aphasia
slowly progressive expressive language dysfunction
Most common presenting symptom of progressive nonfluent aphasia
word-finding difficulty; over time, language deteriorates with decreasing fluency and eventually pt becomes mute
On imaging, progressive nonfluent aphasia:
asymmetric brain atrophy affecting LEFT FRONTAL LOBE
progressive loss of naming ability and loss of ability to understand meaning of words
What type of aphasia is semantic dementia, fluent or non-fluent
fluent, speech is effortless but empty in content
On imaging, semantic dementia:
atrophy of temporal lobes on left
Prion disease, name
Creutzfeldt-Jacob Disease (CJD) -- a group of neurodegenerative disorders
timing characteristics of prion diseases
long incubation periods but rapidly progressive once clinical symptoms begin
3 ways to acquire prion dz
inherited, sporadically, or infectious
Age of onset of CJD
Clinical findings of CJD
rapidly progressive dementia, cortical dysfunction; myoclonic jerks (startle myoclonus), ataxic gait and incoordination, psychiatric abnormalities, akinetic mutism (sleep wake cycles but while awake, mute and immobile)
Etiology of prion dz
abnormal structure and folding of prion protein PrP; changes from normal alpha helical form PrPc to beta-pleated sheet form PrPsc
What matter of the brain does PrPsc accumulate in? What does this produce?
in gray matter --> neuronal loss, gliosis, vacuolation of neuropil --> "spongiform" changes
On autopsy of pt with prion dz, what does brain look like?
filled with HOLES
What CSF protein is present throught nervous system of pt with CJD?
EEG findings of prion dz
periodic sharp wave complexes
MRI of prion dz
increased DWI signal intensity along outer cortex, thalamus, basal ganglia particularly caudate
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