|
Basic
Research
|
After conducting
our own research for over 15 years, and keeping track of discoveries
made in other labs, we have developed two hypotheses regarding
brain damage:
- Changes in the connections that allow
neurons to communicate play a major role in the pathophysiology
of hydrocephalus, and
- The formation of "scar" tissue in hydrocephalic
brains prevents recovery.
|
| To test
these hypotheses, we have used several different animal models
to examine the changes that occur in structures that make up
connections between neurons, namely axons,
dendrites,
and synapses,
as well as the chemicals (neurotransmitters)
that convey electrical messages across synapses. These results
have been correlated with molecular
measures of functional changes that signify loss of neuronal
activity. In addition, because the death of neurons can permanently
eliminate connections and promote axonal rearrangements ("plasticity")
in remaining neurons, we continue to examine the role that cell
death plays in hydrocephalus. Finally, by examining changes
that occur in glial
cells that mediate inflammation within the brain, we have begun
to describe the process through which scars (gliosis)
are formed in the damaged hydrocephalic brain. All of our studies
have been conducted on developing brains, so that the time course
of events can be correlated with the maturation of the brain.
|
| It is clear
that many pathological mechanisms operate concurrently as the
brain is compressed and distorted by ventriculomegaly, and only
carefully designed temporal studies that correlate all of these
processes will unravel the relationships that exist between these
mechanisms. Nevertheless, it is still possible to subdivide these
processes into Primary
mechanisms, which generally occur during early stages of hydrocephalus,
and Secondary
mechanisms, which usually appear later during the progression
of ventriculomegaly and most likely are caused by one or more
of the Primary mechanisms. |
| The overall goal of our
basic research program is to improve the outcome for patients
with hydrocephalus. We can do this by concentrating on several
major aspects of hydrocephalus: |
| The
Role of Neuron Cell Death on Outcome |
| The
Role of Glial "Scar" Formation on Outcome |
| The
Role of Altered Neuron Connections on Outcome |
| Visual
System Changes and Their Impact on Learning Disablities |
| Determining
the Point of Irreversible Damage - Early vs. Late Shunting |
| Effects
of Hydrocephalus on the Reproductive System |
| Axonal
Damage and Neuron Tolerance to Ischemia |
| Mathematical
Modeling of CSF Changes in Communicating Hydrocephalus |
Hydrocephalus
Home 
