Dementia is considered to be a distinct disease separate from Alzheimer’s disease (AD). Among other things, AD is associated with significant atrophy (shrinkage) of the brain as seen in the picture below, as well as characteristic pathology (disease), such as beta amyloids, tau proteins, amyloid plaques and neurofibrillary tangles. The problem is that these pathologies can only be seen on autopsy, therefore, differential diagnosis is difficult in the living.
Nonetheless, as we continue to unravel the mystery about both conditions the lines of distinction are beginning to blur, including pathological differences. Both share similar signs and symptoms. They also share similar causes related to circulation and blood flow in the brain, and they share similar pathology.
In addition to AD, dementia is associated with other neurodegnerative conditions as well including: Parkinson’s disease, Lewy body dementia, Pick’s disease, amyotrophic lateral sclerosis (ALS), Huntington’s chorea and multiple sclerosis to name a few. Moreover, multiple sclerosis is commonly associated with cog fog, in which patients complain of loss of cognitive functions, which includes memory similar to mild dementia. Cog fog is in fact, one of the major causes of occupational disability and unemployment due to MS.
Circulation, Amyloid Plaques and Neurofibrillary Tangles
According to a paper published in 1999 in the Journal of Alzheimer’s Disease and Related Disorders, there is an overwhelming amount of evidence to suggest that the pathological process that leads to the destruction of nerves in the brain seen in AD involves more than just the characteristic amyloid plaques and neurofibrillary tangles, which are considered to be the hallmark signs of Alzheimer’s. It further states that according to a review of various data collected from many sources that more than thirty percent of the cases of AD showed signs of pathology of the blood vessels of the brain. Conversely, certain vascular lesions, such as from amyloid plaques, small blood vessel disease, and white matter (myelin) lesions surrounding the veins (perivenular) are evident in almost all cases of Alzheimer’s disease.
Interestingly, as far as the white matter lesions are concerned, they tend to be in the periventricular areas. The ventricles are the chambers in the brain that contain cerebrospinal fluid. The periventricular areas are the areas of the brain surrounding the ventricles. In this regard, perivenular and periventricular hyperintensity signals due to degeneration of myelin in the brain are one of the hallmark signs of multiple sclerosis. In other words, the white matter lesions of MS tend to be found next to the larger veins surrounding the ventricles of the brain.
It remains to be determined whether the vascular lesions seen in dementia and Alzheimer’s are simply coincidental, or if they are, in fact, the cause of the degenerative processes and subsequent disease. Although systemic vascular influences such as hypertension (high blood pressure), coronary (heart) artery disease, and other cardiovascular disturbances may be responsible for the pathology seen in Alzheimer’s, it is equally intriguing that about one third of patients diagnosed with vascular dementia will have AD type pathology at autopsy. In other words, patients with vascular dementia, such as multi infarct dementia, often have amyloid plaques and neurofibrillary tangles similar to Alzheimer’s disease.
Trauma and Dementia
In addition to problems with circulation, trauma also appears to play a role in dementia and (AD). It’s exact role, however, isn’t clear. In particular, scientists strongly suspect that dementia and AD are related to head trauma. But as yet their suspicions are not yet fully confirmed and remain controversial. What’s particularly puzzling to researchers about the connection between head trauma, dementia and AD is that the signs and symptoms of the conditons generally show up twelve to sixteen years later. Nevertheless, scientists suspect certain similar mechanisms are involved in head trauma cases as those seen in the more obvious types of traumatic brain injuries. Among other things, traumatic brain injuries are associated, for example, with diffuse axonal injuries. Diffuse axonal (axon is part of a nerve cell) injuries show up as diffuse hyperintensity signals on brain scans. Typically, however, the affects of traumatic brain injury and diffuse axonal injury appear soon after the accident, so the connection is quite clear. What’s less clear, is why dementia and AD show up over a decade later.
Basically, the exact cause of both conditions remains a mystery. We do know, however, that blood flow and circulation is important to all the tissues of the body but it is especially critical to the health of the brain and cord. The brain and cord, similar to the heart, are highly sensitive to blood flow.
Nerve cells start to die shortly after being deprived of oxygen. Neurosurgeons surmized long ago that one of the likely causes of brain and cord sensitivity to decreases in blood flow is due to the chemical makeup of cerebrospinal fluid (CSF). It’s a separate subject I will discuss as this site develops.
In brief, fluids between cells in the body are called interstitial fluids. Interstitial fluids typically move through lymph vessels in the body. Edema (swelling) occurs when interstitial fluids back up. In the brain, the interstitial fluid is called CSF. In contrast to the rest of the body the brain has no lymph vessels. Instead, CSF flows through special CSF pathways in the brain called the ventricles, perivasular spaces (also known as the Verchow-Robinson spaces), cisterns and subarachnoid spaces.
Traumatic brain injuries are often associated with ruptured blood vessels that cause bleeding which increases interstitial fluids and consequently causes edema in the brain. Conversely, in the rest of the body, colloids, which are proteins in the interstitial fluids and lymph vessels, act like salt and attract and move water through the lymphatic system. They play an important role in preventing edema.
In contrast to interstitial fluids and lymph in the rest of the body, CSF has far fewer colloids. Among other things, the lack of colloids in CSF makes it more difficult to remove edema in the brain. Edema in turn creates back pressure against oxygenated arterial blood flow. Thus the chemical makeup of CSF makes it much more difficult for the brain to recover from ischemia (lack of blood flow), Ischemia causes a decrease in oxygen delivery to the affected nerves.
In addition to the more obvious traumatic type brain injuries that often result in coma, head injuries and concussions that cause partial or temporary loss of consciousness can also result in edema. Furthermore, getting “knocked unconscious” is the consequence of a mini stroke that temporarily cuts off blood flow to the brain without rupturing blood vessels. Nonetheless, the chemical nature of CSF makes it more difficult to recover from this type of loss of blood flow as well.
The Craniocervical Spine, Blood and CSF Flow
In addition to ischemia and edema, trauma can also affect cerebrospinal fluid flow. As mentioned above, CSF is the interstitial fluid of the brain. Technically speaking, hydrocephalus (water on the brain) occurs when CSF backs up and its volume in the brain increases.
In light of the above, twenty percent of the blood flow to the brain passes through the vertebral-basilar arteries, which pass through openings in six of the seven vertebrae of the cervical spine and from there into a canal between the atlas and skull, and finally through the foramen magnum in the skull. Furthermore, the venous drainage system of the brain, as a result of upright posture, also passes through the foramen magnum, as well as other openings in the base of the skull and empties into the vertebral venous plexus in the upper cervical spinal canal. Lastly, CSF flows between the cisterns of the brain and the subarachnoid space of the cord in the upper cervical spine.
Now consider the vulnerability of the human cervical spine to trauma. Futhermore, although not always, head and neck trauma often occur together. In fact, they are more likely to occur together than not. It is hard to separate them. It is possible that one of the likely causes of dementia and Alzheimer’s disease is injuries that causes degeneration in the cervical spine as it ages.
Injuries to the upper cervical spine are common in humans. Bipedalism and upright posture with a large head that sits on a small neck makes humans susceptible to whiplash simply from slips and falls.
Over time, aging, injuries and degeneration of the spine can lead to compression of the contents of the foramen magnum and upper cervical spinal canal. This could lead to chronic decreases in arterial blood flow to the brain, as well as decreased drainage capacity of the brain. Lastly, it could also lead to chronic back ups of CSF in the brain and a condition called normal pressure hydrocephalus or NPH.
There is a reason why a neurodegenerative disease shows up in an individual’s life at the time that is does. MS shows up in midlife (or not too long after a trauma), followed by Parkinson’s disease and AD and dementia show up much later. Dementia and Alzheimer’s start to show up in life when the circulatory system is in decline. Degeneration of the spine compounds the problem. When the degenerative process crosses a certain threshold it starts to affect the contents of the foramen magnum and spinal canal, which includes the vertebral arteries, the vertebral veins and the subarachnoid space for CSF flow in the brain and cord.
Degeneration of the upper cervical spine can lead to chronic ischemia (decreased arterial blood flow), edema (swelling) and normal pressure hydrocephalus (back up of CSF in the brain). Aging by itself causes all aspects of the body to breakdown. Accidents and injuries simply speed up and complicate the degenerative process.
If you found this page interesting you might also check out the page on Parkinson’s Disease, Dementia, Neck Injuries and Sports.