Question:
I consider bipolar disorder a neurological disease because it is a disease
of the brain which is part of the CNS. Am I wrong?
Answer:
I think it is a matter of semantics. Bipolar Disorder has a
pathophysiological origin...in the brain. Here is an article:
From:
http://bipolar.about.com/health/bipolar/library/press/bl-umich-10-2-00.h ANN ARBOR, MI - People with bipolar disorder have an average of thirty
percent more of an important class of signal-sending brain cells,
according to new evidence being published by University of Michigan
researchers.
The finding, published in the October 2000 issue of the American Journal
of Psychiatry, solidifies the idea that the disorder has unavoidable
biological and genetic roots, and may explain why it runs in families.
The discovery is the first neurochemical difference to be found between
asymptomatic bipolar and non-bipolar people. It could help the
understanding and treatment of a disease that affects as much as 1.5
percent of the population. Bipolar disorder has in the past been known
as manic depression.
"To put it simply, these patients' brains are wired differently, in a
way that we might expect to predispose them to bouts of mania and
depression," says Jon-Kar Zubieta, M.D., Ph.D., assistant professor of
psychiatry and radiology at the University of Michigan Health System.
"Now, we must expand and apply this knowledge to give them a treatment
strategy based on solid science, not on the current method of trial and
error. We should also work to find an exact genetic origin, and to
relate those genetic origins to what is happening in the brain."
Bipolar disorder is marked by wild, cyclical mood swings, which
typically begin in a person's late teens or twenties and strike men and
women with equal frequency. Its milder, type II form causes depression
alternating with hyperactivity, while the more severe type I disorder
produces frenzied, even psychotic episodes that may send the patient to
the hospital, followed by deep, crippling depressions. Current treatment
uses a mix of mood-stabilizing, anti-psychotic and antidepressant drugs,
but patients and physicians often struggle to strike the right
combination.
Zubieta and his colleagues made the discovery in 16 patients with type I
bipolar disorder using a brain imaging technique called positron
emission tomography, or PET. The scans let them see the density of cells
that release the brain chemicals dopamine, serotonin and norepinephrine.
These monoamines, as the chemicals are called, send signals between
brain cells, or neurons. They're involved in mood regulation, stress
responses, pleasure, reward, and cognitive functions like concentration,
attention, and executive functions. Scientists have hypothesized their
role in bipolar disorder for decades, but have never proven it.
The new University of Michigan result points to a clear difference in
the density of monoamine-releasing cells in the brains of bipolar people
even when they are not having symptoms. Zeroing the PET scanner in on
areas of the brain where monoamine-releasing cells are concentrated, the
team looked for the faint signal of a weakly radioactive tracer, DTBZ,
which they had injected into the bloodstream of the 16 participants and
16 people without bipolar disorder.
DTBZ binds only to a protein called VMAT2 inside monoamine-releasing
cells, making it a good tracking device for the density of those cells.
It is also often used in PET scanning to study Parkinson's disease,
which is characterized by a severe shortage of cells that produce
dopamine. On PET scans, DTBZ density - and therefore monoamine cell
density - can be quantified by the amount of radioactive signal present
in different areas.
By looking at the intensity of the DTBZ signal in all the subjects'
brains, the University of Michigan team found that bipolar patients
averaged 31 percent more binding sites in the region known as the
thalamus, and 28 percent more in the ventral brain stem. In the
thalamus, bipolar women actually had levels nearing those of healthy
comparison subjects, but bipolar men had a 42 percent higher binding
rate, suggesting that there may be specific biological causes for the
clinical differences in the course of the illness in men and women.
Adding in the results of functional tests, they found that the more
monoamine cells patients had, the lower their scores on tests of
executive function and verbal learning. This finding confirms earlier
results from research at the University of Michigan, and suggests that
the altered brain chemistry due to the excess monoamine cells may
directly impact the patients' cognitive and social function.
The study was carefully designed to produce consistent results. It
compared brain scans and neuropsychological test results from bipolar
disorder I patients who were using medications to control their
symptoms, and healthy subjects matched to the bipolar subjects for age,
sex, ethnicity, handedness and other factors. Careful physical and
psychiatric exams ruled out differences caused by other variables.
Now, Zubieta and his colleagues hope their initial finding will lead to
further research on brain chemistry and bipolar disorder. Specifically,
more study is needed to examine which kinds of monoamine cells are
involved - Zubieta especially suspects those that produce serotonin and
norepinephrine. Those findings could help define specific subtypes of
bipolar disorder, and aid development of medications and drug
combinations that target a specific patient's personal brain chemistry
to alleviate symptoms.
Genetic research, too, will be needed to find out why bipolar brains
grow more than the usual allotment of such cells. Bipolar disorder I has
a strong but still unknown tie to DNA; studies of identical twins show
that if one twin has it, the other has an 80 percent chance of having
it, too. Zubieta is hopeful that genetic markers will one day be found
that can help people know their risk of developing bipolar disorder.
A combination of both genetic research and neuroimaging studies would
help define both the genetic components of this illness, and their
relationship with the expression of specific brain chemical markers in
specific patients.
The University of Michigan is launching a new trial that will enroll
patients who have just been diagnosed with bipolar disorder, and those
with a family history of the disease that puts them at higher risk.
