Chapter 4: Brain Plasticity Flashcards
stroke or cerebrovascular accident 136
A common cause of brain damage, especially in older people, is temporary interruption of normal blood flow to a brain area during a stroke, also known as a cerebrovascular accident.
closed head injury 136
In young people, the most common cause is closed
head injury, a sharp blow to the head that does not puncture the brain. The effects of closed head injury depend on severity and frequency. Many, probably most, children and young adults sustain at least a mild blow to the head from falling off a bicycle or similar accident, from which they recover within a few days.
edema 136
Both ischemia and hemorrhage lead to many of
the same problems, including edema (the accumulation of fluid), which increases pressure on the brain and the probability of additional strokes. Both ischemia and hemorrhage also impair the sodium–potassium pump, leading to an accumulation of sodium inside neurons.The combination of edema and excess
sodium provokes excess release of the transmitter glutamate, which overstimulates neurons,
damaging both neurons and synapses.
hemorrhage 136
The less common type is hemorrhage (HEM-oh-rage), the result of a ruptured artery. Effects of strokes vary from barely noticeable to immediately fatal. In hemorrhage, they are flooded with blood and excess oxygen, calcium, and other chemicals.
ischemia 136
The more common type of stroke is ischemia (iss-KEE-meuh), the result of a blood clot or other obstruction in an artery. In ischemia, the neurons deprived of blood lose much of their oxygen and glucose supplies.
tissue plasminogen activator
(tPA) 137
A drug called tissue plasminogen activator (tPA)
breaks up blood clots. To get a benefit, a patient should receive tPA quickly, at least within 4.5 hours after a stroke. Emergency wards have improved their response times, but the limiting factor is that most stroke victims don’t get to the hospital quickly enough. The usual decision is to give the tPA. Hemorrhage is less common and usually fatal anyway, so the risk of making a hemorrhage worse is small compared to the hope of alleviating ischemia.
diaschisis 138
Diaschisis refers to the decreased activity of
surviving neurons after damage to other neurons. If diaschisis contributes to behavioral deficits following brain damage, then increased stimulation should help. (This stimulation should not occur during the first day or two after the stroke, while neurons may be dying from excess stimulation, but instead during a later period of recovery.)
collateral sprouts 139
After a cell loses input from an axon, it secretes neurotrophins that induce other axons to form new branches, or collateral sprouts, that take over the vacant synapses. In the area near the damage, new synapses form at a high rate, especially for the first two weeks. Is collateral sprouting helpful or harmful? It depends on whether the sprouting axons convey information s imilar to those that they replace.
denervation supersensitivity 140
Neurons make adjustments to maintain a nearly constant level of arousal. After learning strengthens one set of synapses, other synapses weaken. Conversely, if a certain set of synapses. becomes inactive—perhaps because of damage elsewhere in
the brain—the remaining synapses become more responsive, more easily stimulated. This process of enhanced re sponse, known as denervation supersensitivity or receptor supersensitivity,
has been demonstrated mostly with dopamine synapses.
phantom limb 141
Physicians have long noted that most people with amputations experience a phantom limb, a continuing sensation of an amputated body part. That experience can range from occasional tingling to intense pain, and from occasional to constant experience.
deafferented 142
Consider an animal that incurred damage to the sensory nerves linking a forelimb to the spinal cord. The animal no longer feels the limb, although the motor nerves still connect to the muscles. We say the limb is deafferented because it has lost its afferent (sensory) input.
Immediate Treatment
- The most effective known method of preventing brain
damage after strokes in laboratory animals is to cool the brain. Cooling protects the brain after ischemia by reducing overstimulation, apoptosis, and inflammation. People can be cooled safely as far as 33°C (91°F). - Another procedure might surprise you: Exposure to
cannabinoids (the chemicals found in marijuana) minimizes the damage caused by strokes in laboratory animals. You might wonder how anyone thought of trying such a thing. The theoretical rationale was that cannabinoids decrease the release of glutamate.
