Muscular & Cerebral Atrophy
Atrophy is the progressive degeneration or shrinkage of muscle or nerve tissue.
In multiple sclerosis (MS), two types of atrophy are common: muscle atrophy (due
to disuse of specific muscles) and brain or cerebral atrophy (due to demyelination
and destruction of nerve cells).|
When a person complains of muscle weakness, the doctor checks muscles for bulk
and texture and for tenderness. Muscles are also checked for twitches and
involuntary movements, which may indicate a nerve disease rather than a muscle
disease. Doctors look for wasting away of muscle (atrophy), which can result
from damage to the muscle or its nerves or from lack of use (disuse atrophy), as
sometimes occurs with prolonged bed rest. Doctors also look for muscle
enlargement (hypertrophy), which normally occurs with an exercise such as weight
lifting. However, when a person is ill, hypertrophy may result from one muscle
working harder to compensate for the weakness of another.
Cerebral atrophy is a common feature of many of the diseases that affect the
brain. Atrophy of any tissue means loss of cells. In brain tissue, atrophy
describes a loss of neurons and the connections between them. Atrophy can be
generalized, which means that all of the brain has shrunk or it can be focal,
affecting only a limited area of the brain. The result of this type of atrophy
can be a decrease of function in the affected area of the brain. If the cerebral
hemispheres are affected, conscious thought and voluntary processes may be
Cerebral Atrophy Symptoms:
This is characterized by a progressive impairment of memory and intellectual
function that is severe enough to interfere with social and work skills. Memory,
orientation, abstraction, ability to learn, visual-spatial perception, and
higher executive functions such as planning, organizing, and sequencing may also
These can take different forms, appearing as disorientation, repetitive
movements, loss of consciousness, or convulsions.
A group of disorders characterized by disturbances in speaking and understanding
language. Receptive aphasia causes impaired comprehension. Expressive aphasia is
reflected in odd choices of words, the use of partial phrases, disjointed
clauses, and incomplete sentences.
Muscle atrophy is the wasting or loss of muscle tissue. There are two types of
muscle atrophy: disuse and neurogenic.|
The first type of muscle atrophy is disuse atrophy
and occurs from a lack of physical exercise. In most people, muscle atrophy is
caused by not using the muscles enough. Those with sedentary jobs, medical
conditions that limit their movement, or decreased activity levels can lose
muscle tone and develop atrophy. Those who are bedridden can have significant
muscle wasting. This type of atrophy can usually be reversed through exercise
and/or better nutrition.
The second and most severe type of muscle atrophy is
neurogenic atrophy. This occurs when there's an injury to, or disease of
a nerve such as with MS. This type of muscle atrophy tends to occur more suddenly
than disuse atrophy. This type of atrophy can't usually be reversed since there
is actual physical damage to the nerve. Neuromuscular Electrical Stimulation
(NMES) has been used as a form of physical therapy that applies electrical
muscle stimulation via small electrical impulses to nerves and muscles in an
effort to cause involuntary muscle contractions. The electrical impulses are
sent by electrodes placed on your skin over the muscle or muscles.
Although people can adapt to muscle atrophy, even minor muscle atrophy causes
some loss of movement or strength. Symptoms of muscle atrophy may include:
||Balance problems, difficulty walking, and falls
||Difficulty with speaking and swallowing
||Gradual memory loss
||Impaired balance and coordination
||Loss of muscle coordination
||Numbness or tingling in arms or legs
||Progressive loss of movement
||Progressive weakness and numbness in the legs
The loss of brain tissue, called brain atrophy, is a normal part of aging,
but MS accelerates the process. Such atrophy is a critical indicator of
physical and cognitive decline in MS, yet because measuring brain atrophy
is expensive and complicated, it's done primarily in research settings.|
The biological basis of gray matter atrophy in MS is not well understood, but
gray matter damage seems to be the most critical factor leading to permanent
disability. Until now, it was thought that the lesions or plaques observed in
the white matter were the cause of the damage to the brain. New data indicates
that these lesions account for only 30% of the atrophy in the gray matter; other
unexplained neurodegenerative mechanisms are therefore also implicated.
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Principal Cause is Unknown
MS is a chronic inflammatory neurodegenerative disease of the central nervous system
(CNS) that affects the brain and spinal cord. It's the most common chronic neurologic
disease in young people and adults in Europe and affects approximately 2.5 million
people throughout the world. The study was published in the journal
Archives of Neurology (66(2):173-9) and was carried
out by the team of Dr. Pablo Villoslada at the University of Navarre. Last December, these
researchers joined Hospital Clínic, Barcelona-IDIBAPS. Until now, it was thought that the
atrophy seen in the brains of patients with MS was caused by the plaque in the white matter.
The new results show that these plaques explain only 30% of the lesions.
Until now it was assumed that MS predominantly affected myelin, a fat that sheaths the
nerves. It was thought that the plaques that form in the myelin were directly responsible
for the atrophy of the grey matter. This study was designed to determine whether the
loss of volume–atrophy–in the brain’s structures was related to the presence of lesions
or cuts in the nerves connected to them.
The researchers analyzed the brains of 81 people (61 with MS and 20 healthy people) using
magnetic resonance imaging (MRI) and a morphometric method (volumetry). The study focused
on the optical pathway, starting with the hypothesis that lesions in this part of the
brain, and in no other, correlate with atrophy of the occipital cortex and the lateral
geniculate nucleus (LGN), the main centers for processing visual information. The results
indicate that the lesions in the white matter of the nerves originating in the LGN explain
up to 28% of the variation in volume. Atrophy of the occipital cortex did not correspond
to the presence of lesions in the optical pathway, probably because it is associated with
many other pathways.
Thus, although the sclerotic plaques in the nerves contribute significantly to the atrophy
of the grey matter, the remaining 72% must still be explained. The data suggest that other
neurodegenerative processes are involved. Because atrophy of the grey matter is the main
cause of the progressive form of the disease and its severe sequelae, it's important to
gain a better understanding of the principal mechanism of the damage, apart from the classic
plaques, in order to be able to apply this knowledge to treating the disease.
Cerebral Atrophy and Depression
A recent study reported on the
UCLA Newsroom, looks at brain atrophy as a cause
of depression for those with MS. Adding to all that ails people managing their
MS is depression ― for which MS sufferers have a lifetime risk as high as 50%.
Yet despite its prevalence, the cause of this depression is not understood. It's
not related to how severe one's MS is, and it can occur at any stage of the
disease. That suggests it's not simply a psychological reaction that comes from
dealing with the burden of a serious neurologic disorder.
Now, in the first such study in living humans, researchers at UCLA suggest a
cause, and it's not psychological, but physical: atrophy of a specific region of
the hippocampus, a critical part of the brain involved in mood and memory, among
Reporting in the early online edition of the journal Biological Psychiatry,
senior study author Dr. Nancy Sicotte, a UCLA associate professor of neurology,
Stefan Gold, lead author and a postdoctoral fellow in the
UCLA Multiple Sclerosis Program, and colleagues
used high-resolution magnetic resonance imaging (MRI) to identify three key
sub-regions of the hippocampus that were found to be smaller in people with MS
when compared with the brains of healthy individuals.
The researchers also found a relationship between this atrophy and hyperactivity
of the hypothalamic-pituitary-adrenal (HPA) axis, a complex set of interactions
among three glands. The HPA axis is part of the neuroendocrine system that
controls reactions to stress and regulates many physiological processes. It's
thought that this dysregulation may play a role in the atrophy of the
hippocampus and the development of depression.
"Depression is one of the most common symptoms in patients with multiple
sclerosis," Gold said. "It impacts cognitive function, quality of life, work
performance and treatment compliance. Worst of all, it's also one of the
strongest predictors of suicide."
The researchers examined three sub-regions of the hippocampus. They imaged 29
patients with relapsing-remitting MS (RRMS) and compared them with 20 healthy
control subjects who did not have MS. They also measured participants' cortisol
level three times a day; cortisol is a major stress hormone produced by the HPA
axis that affects many tissues in the body, including the brain.
In addition to the difference between MS patients and healthy controls, the
researchers found that the MS patients diagnosed with depression showed a smaller
CA23DG sub-region of the hippocampus, along with excessive release of cortisol
from the HPA axis.
"Interestingly, this idea of a link between excessive activity of the HPA axis
and reduced brain volume in the hippocampus hasn't received a lot of attention,
despite the fact that the most consistently reproduced findings in psychiatric
patients with depression (but without MS) include hyperactivity of the HPA axis
and smaller volumes of the hippocampus," Sicotte said.
"So the next step is to compare MS patients with depression to psychiatric
patients with depression to see how the disease progresses in each," she said.