Do You Think Mr. C’s Memory Problems Are Stroke Related?

Due to the rapid onset of memory loss and behavioural
change, Mr. C’s memory problems are more than likely a
result of the stroke. The term vascular dementia is used
to describe dementia with onset after stroke for which
no other explanation can be found. Memory loss after
stroke occurs in approximately one third of all stroke
victim(Maud, 2006). According to his physical symptoms
the stroke probably occurred in the right hemisphere
(left sided weakness) and the patient’s suspiciousness
points to a frontal or temporal lobe site of injury.
Memory impairments after stroke are often overshadowed
by the physical implications and are not recognized
until later. 

  Other possibilities    1)Depression- as a direct
result of the impact of the stroke on the person’s
self-concept or changes in blood flow (increase to
frontal area in response to damage).

2)Alzheimer’s Disease- as described below

3)Hyperglycemia and/or electrolyte imbalances can worsen
mood and interfere with memory

4)Seizures- such as absence seizures can occur acutely
as a result of inflammation or chronically as a result
of damage to brain tissue. This can result in memory
loss and possibly mood changes depending on the area of
brain affected. 

5)Brain Metastases- unlikely as brain metastases tend to
originate in the lung as opposed to the GI system or
liver. There is no mention of lung metastases.


How Would The Pathophysiology Be Different For Alzheimer
Dementia?


Stroke

In stroke, ischemia of brain tissues results when there
is a sudden impairment of circulation to the affected
area of the brain. Strokes can either be cerebral
infarctions where vascular occlusion results in cell
death beyond the point of occlusion, or cerebral
hemorrhage where a blood vessel bursts depriving the
brain tissues of circulation beyond that point.  In
either case brain tissues suffer from ischemia and
necrotic tissues may result. The area of the brain
affected will determine the types of deficits expressed.


Alzheimer’s disease (AD)

AD is a common cause of structural and functional
changes which eventually lead to dementia. Its aetiology
is unknown, but four possible theories are: 

1)Loss of neurotransmitter stimulation by choline
acetyltransferase

2)Mutation for encoding amyloid precursor protein

3)Alteration in apolipoprotein E, which binds beta
amyloid

4)Pathologic activation of N-methyl-D-aspartate
resulting in an influx of calcium (McCance & Huether,
2006).

Brashers and Forshee (2006) explain that AD has been
associated with mutations in chromosomes 19 and 21. 
Environmental toxins, viruses and other infectious
particles have been implicated as possible triggers.

Abnormal amyloid proteins and apolipoprotein E molecules
accumulate in the brain and result in characteristic
neuritic plaques and neurofibrillary tangles. These
structural deformities are found in the memory areas of
the cortex and hippocampus of those with Alzheimer’s
disease. Functional changes include decreased levels of
the neurotransmitter acetylcholine and increased levels
of the excitotoxins glutamate and aspartate (which bind
to N-methyl-D-aspartate receptors creating neurotoxic
effects).


References:

Brashers, V.L. & Forshee, B.A. (2006).  Algorithm: 
Alzheimer disease.  Retrieved May 21, 2007 from:
http://coursewareobjects.elsevier.com/objects/mccance5e_v1/McCance/Module10/M10L09S75.html?hostType=undefined&authorName=Mccance&prodType=undefined

Maud, A.  (2006). Memory loss after stroke [Electronic
version]. American Academy of Neurology, 67(8).
Retrieved May 22, 2007 from:
www.neurology.org/cg/content/full/67/8/E14

McCance, K. L., & Huether, S. E.(2006). Pathophysiology:
The biologic basis for disease in adults and children.
St. Louis, MO: Elsevier Mosby.

National Institute on Aging (2006). Alzheimer’s
information. Retrieved May 21, 2007 from:
http://www.nia.nih.gov/Alzheimers/AlzheimersInformation/GeneralInfo/

National Institute of Neurological Disorders and Stroke
(2007). Alzheimer’s disease. Retrieved May 21, 2007
from:
http://www.ninds.nih.gov/disorders/alzheimersdisease/alzheimersdisease.htm