Are Mr. C’s memory problems stroke related or due to pathophysiology of Alzheimer’s disease?

Before I could answer this question with certainty I would need considerably more information. Are there any diagnostic test done, what lab values are there? Many factors can mimic dementia like behavior for example an urinary tract infection especially if it becomes septic, his out of control sugar levels especially low sugars could cause him to be confused and have poor memory function. Poly pharmacy is another concern with elderly, as the combination of certain medications could be causing the dementia like behavior.

Dementias can result from diseases such as Alzheimer’s, and Parkinson’s disease or from a vascular incident. Dementias are progressive, and deteriorating illness (Rockwood, K., Chisholm, T., 2007).

Alzheimer’s disease cannot be definitely diagnosed until after death, when the brain can be closely examined for certain microscopic changes caused by the disease. Determining the type of dementia remains a difficult task for care provider at times. There is no specific biological marker for Alzheimer’s disease and Computed tomography or magnetic resonance imaging can only detect relatively small infarcts or hemorrhage (Tierney, M, Black, S., Szalai,j., 2001). However, through thorough testing and a “process of elimination,” doctors today can diagnose what they refer to as probable Alzheimer’s disease with almost 90% accuracy.

Differentiating Alzheimer’s disease from Memory disorders cause by a Stroke:

Progressive cerebral atrophy and ventricular enlargement were much greater in Alzheimer’s patients. Cerebral perfusion decreased progressively but diffusely in Alzheimer’s patients, in stroke patients there was only a minimal decline in perfusion. Age-related tissue density decreases were limited to the frontal cortex in stroke patients but also included the parietotemporal cortex in Alzheimer’s patients. In stroke patients, bidirectional changes in cognitive test performance correlated directly with perfusional changes within the frontal white matter, thalamus, and internal capsule. Progressive cognitive declines in Alzheimer are correlated with diffuse cerebral cortical atrophy and perfusional decreases (Meyer, J. , Muramatsu, Mortel, K., et.al, 1995).

With Alzheimer’s disease the research is inconclusive but research is leaning towards an increase in the production of beta-amyloid peptide. This protein is derived from amyloid precursor protein and, when grouped together, it becomes neurotoxic and forms the core of neuritic plaques. Nerve cell loss in selected nuclei leads to neurochemical deficiencies, and the combination of neuronal loss and neurotransmitter deficits leads to the appearance of the dementia syndrome. The destructive aspects include neurochemical deficits that disrupt cell-to-cell communications, abnormal synthesis and accumulation of cytoskeletal proteins (e.g., tau), loss of synapses, pruning of dendrites, damage through oxidative metabolism, and cell death (Graham, T., 2004).

The following may be used to help make a diagnosis of Alzheimer’s disease:

Mini-Mental State Examination

This is a very brief test that the doctor can use to test a person’s problem solving skills, attention span, counting skills and memory. It will give the doctor insight into whether there has been damage to different areas of the brain.

Causes of memory loss
Many primary neurological or psychiatric diseases, and some general medical disorders with secondary neurological complications, for example diabetes, respiratory failure or liver failure, may cause memory impairment or even frank dementia.

In clinical practice, however, the two most common are Alzheimer’s disease and depression, and these merit consideration in every patient with memory complaint. These are not mutually exclusive.

Alzheimer’s disease typically presents with failure to recall recent day-to-day events or activities (episodic or autobiographical amnesia) but often with well-preserved remote memory (the temporal gradient of amnesia).

In contrast, patients with cognitive impairment associated with depression, sometimes known as ‘pseudo-dementia’, may give a very exact account of their memory failures.

Biological (neurovegetative) symptoms may be apparent, such as social withdrawal, apathy and sleep disturbance, all of which may contribute to poor memory function.

Impaired sleep (increased latency to sleep onset, frequent nocturnal waking with difficulty getting back to sleep) is a common finding in the non-demented clinical population, whether or not they have symptoms of depression.

If depression is suspected, a trial of antidepressant medication is indicated, for at least six months.

Differential diagnosis of memory loss
Neurodegenerative diseases

· Alzheimer’s disease +/- cerebrovascular disease (very common)

· Parkinson’s disease dementia/dementia with Lewy bodies (quite common)

· Frontotemporal dementias (rare)

· Huntington’s disease (rare)

· Prion diseases (very rare)

Primary psychiatric disorders

· Depression +/- anxiety (very common)

· Schizophrenia

· Vascular dementias (rare in isolation)

· Alcohol-related dementia or Wernicke-Korsakoff syndrome

· Epilepsy +/- antiepileptic drug therapy

· Inflammatory CNS disorders, such as multiple sclerosis

· Structural brain disease, such as tumors +/- radiotherapy

· Infection, such as sequelae of herpes simplex encephalitis

· Primary sleep-related disorders

‘Reversible causes’ (very rare)

· Neurosyphilis

· Hypothyroidism

· Vitamin B12 deficiency

A person with Alzheimer’s may have years of comfortable, good life remaining. As most persons with Alzheimer’s are older, life may end before the slow progress of the brain disorder seriously interferes with the quality of life. Working to slow the disease and improve its symptoms is the important goal in Alzheimer’s.

The pathophysiology of a cerebral vascular accident: There are various forms of CVA’s the two categories are occlusive or hemorrhagic. Athero- thrombotic occlusion of larger arteries (e.g., carotid, middle cerebral, basilar) is not only the most common cause of primary large vessel occlusive cerebral vascular disease, but also is the most common cause of stroke (Desmond, D., Moroney, J., et. Al., 2002).

After primary large vessel occlusive disease, embolism is the most common cause of stroke. Most embolic strokes are due to cerebral arterial atherothrombosis, in which a larger thrombus and is carried to other places in the cerebrovasculature. Cerebral emboli may also arise from other cardiogenic sources and deep vein thrombosis (Desmond, D., Moroney, J., et. Al., 2002).

Primary small vessel cerebral vascular disease most prominently causing lacunar strokes arises from microatheroma of an influx of fat-like materials (lipohyalinosis). In humans, it appears that 5 to 10 minutes of complete occlusion is required for irreversible brain damage. In actuality, most strokes do not involve a complete occlusion of blood flow, but even a partial occlusion, if allowed to continue for a sufficient time, may produce irreversible brain damage (Desmond, D., Moroney, J., et. Al., 2002).

Approximately 30% of strokes are caused by cerebral embolism, a type of ischemic stroke that occurs when circulation to a portion of the brains is blocked by an embolus (clot) originating elsewhere in the circulation, most frequently from the heart or from the cervical portion of the carotid artery. Part or all of the embolus is carried through the bloodstream until it lodges within an artery too small to allow passage, preventing the blood behind it from passing as well. Embolic strokes, which are more common in younger patients, develop rapidly, with maximum deficit usually present within seconds to minutes.

Hemorrhagic stroke, which accounts for approximately 20% of all strokes, may be due to intracerebral hemorrhage or subarachnoid hemorrhage. An intracerebral hemorrhage (also called a parenchymal hemorrhage) occurs when a diseased artery within the brain ruptures, flooding the surrounding brain tissue with blood. The major risk factor for intracerebral hemorrhage is hypertension. Most signs and symptoms associated with intracerebral hemorrhage are caused by the compression of brain structures and blood vessels (Desmond, D., Moroney, J., et. Al., 2002).

Subarachnoid hemorrhage (bleeding into the skull or cranium that occurs when a blood vessel on the surface of the brain ruptures and bleeds into the meninges) usually follows the rupture of an aneurysm or an arteriovenous malformation (Desmond, D., Moroney, J., et. Al., 2002).

Alzheimer patients are more likely to be impaired than patients with vascular dementia in concerns with episodic memory. Patients with vascular dementia were more likely impaired with semantic memory, executive/attentional functioning, and visuospatial and perceptual skills. Subcortical vascular dementia and Alzheimer’s disease produce distinctive profiles of cognitive impairment that can assist with diagnosis, but many of the neuropsychological deficits thought to characterise Alzheimer’s disease are also found in subcortical vascular dementia making diagnosis that much more difficult for the practitioner (Meyer, J. , Muramatsu, Mortel, K., et.al, 1995).

Memory loss commonly occurs as a result of the loss of nerve cells in the brain. When memory loss is so severe that it interferes with normal daily functioning, it is called dementia. People with dementia may have difficulty learning new things or remembering names of people they just met. They may get lost in places that were previously very familiar or have trouble finding words. The term "mild cognitive impairment" is used for a common condition in elderly people in which the memory problem is usually mild and does not interfere with normal daily activities. Most people with mild cognitive impairment do not develop a severe memory problem or end up developing dementia. There are many things that can cause dementia. One of these is Alzheimer disease (AD), the most common cause of dementia in the elderly. Another is called vascular dementia, caused by brain damage due to strokes. The symptoms of vascular dementia in addition to the memory loss include slow movement, slow thinking, lack of attention, and lack of an ability to do simple tasks. These symptoms are sometimes hard to differentiate from those produced by AD, the most common cause of dementia in the elderly. Symptoms of dementia after stroke can also be hidden by other more obvious stroke manifestations like paralysis, blindness, or lack of awareness. Another problem in recognizing the symptoms of dementia after stroke is that these symptoms can be confused with depression, which is quite common after stroke.

References

Desmond, d., Mororney, J., et.al. (2002). Incidence of dementia after ischemic stroke. Stroke 33:2254

-2262. Retrieved from http://stroke.ahajournals.org/cgi/content/full/33/9/2254

Graham, N.,L., Emery, T., & Hodges, J.R., (2004). Distinctive cognitive profiles in alzheimer’s disease and

subcorticalvascular dementia. Journal of Neurol Neurosurg Psychiatry, 75:61-71. Retrieved from http://www.jnnp.com

Meyer, J.S., Muramatsu, K., et.al. (1995). Prospective CT confirms differences between vascular and

alzheimer's dementia.

Tierney, M., Black, S., et.al. (2001). Recognition memory and verbal fluency differentiate probable alzheirmer disease from subcortical ischemic vascular dementia. Arch Neurol, 58:164-1659. Retrieved from http://archneur.ama-assn.org/cgi/content/abstract/58/10/1654