Download Ch 10 Brain Damage & Neuroplasticity (pt2)

March 20, 2013


Brain Tumors
Cerebrovascular Disorders (Strokes)
 Cerebral Hemorrhage & Ischemia


Closed-Head Injuries
Infections
 Bacterial & Viral



Neurotoxins
Genetic Factors
Programmed Cell Death


Normal human cells have 23 pairs of
chromosomes
An extra chromosome 21 results in Down
syndrome
 Occurs in 0.15% of births
▪ Likelihood increases with maternal age
 Flattened skull & nose, inner eye folds of skin,
short fingers, intellectual impairment & medical
complications





Apoptosis: genetic self-destruct program for
neurons (cell suicide)
Functions in early development by
eliminating extra, unnecessary neurons
Also involved in brain damage
Passive cell death (necrosis) occurs only when
neurons are damaged severely
The majority is due to apoptosis
 Neurons slowly shrivel, die & break down without
inflammation or causing damage to nearby cells





Epilepsy
Parkinson’s Disease
Huntington’s Disease
Multiple Sclerosis
Alzheimer’s Disease


Main symptom is repeated seizures, caused by
chronic brain dysfunction
Different types of seizures
 Convulsions
▪ Motor seizures; involve tremors (clonus), rigidity (tonus) &
loss of balance and consciousness
 Others happen with seemingly no change in behavior


All of the previously discussed causes of brain
damage can cause epilepsy
Often associated with problems at inhibitory
synapses


Diagnosed with scalp
electroencephalography (EEG)
People often experience a weird
psychological change before a
convulsion (epileptic aura)
 Ex: bad smell, déjà vu, hallucination
 Can give a hint of brain area causing
seizures
2 types
1. Partial



Partial seizure does not involve the whole brain
Caused by synchronous burst of neuron firing
Generalized
2.



Entire brain is involved
Grand mal (“classic” seizure)
Petit mal (no convulsions)


Symptoms of a resting tremor, muscular
rigidity, difficulty initiating movement, slow
movement, masklike face
Associated with degeneration of the
substantia nigra in the midbrain
 Primarily of dopaminergic neurons
 So symptoms can be alleviated by L-Dopa
injections (but not permanently)
 Other treatments include dopamine agonists

Another progressive motor disorder
 Late stages involve severe cognitive decline

Onset around age 40
 No cure & usually death within 15 years


Rare
Has a strong genetic basis
 If a parent has it, 50/50 chance child will have it





MS is a progressive disease that attacks the
myelin of axons in the CNS
Eventually causes dysfunction in the axons &
scar tissue develops (sclerosis)
An autoimmune disorder
Symptoms include visual disturbances,
muscular weakness, numbness, tremor &
ataxia (loss of motor coordination)
Genetic & environmental influences


The most common cause of dementia
Likelihood of having it increases with age
 10% of age 65+; 35% of age 85+

Progressive disease
 Early stage: memory decline, attention problems &
personality changes
 Mid stage: confusion, irritability, anxiety, problems
with speech, swallowing & bladder control
 Ultimately terminal

Can only be certain of diagnosis
during autopsy
 Presence of neurofibrillary tangles &
amyloid plaques
Neuroplastic responses to brain damage
1. Degeneration
2. Regeneration
3. Reorganization
4. Recovery of function

 aka neural deterioration
 2 types
1. Anterograde degeneration
 Degeneration of distal segment
▪
▪
(Section of axon between the cut & the synaptic terminal)
Segment no longer gets energy from the cell body
Retrograde degeneration
2.

Degeneration of proximal segment
▪
▪
(Section of axon between the cut & the soma)
If the axon cannot reestablish contact with a target, the
neuron eventually dies


Regrowth of damaged neurons
Not as successful in mammals as in lower
vertebrates & inverts
 Almost nonexistant in CNS of adult mammals


Regrowth from proximal stump 2-3 days after
axonal damage
Does not necessarily mean that function will
be returned

The brain can effectively reorganize itself in
response to damage
 Other areas can compensate for the damaged
area’s function


Ex: blind individuals have little use for visual
cotex, so the auditory & somatosensory
cortex expands into this region, giving them
heightened sensitivity to hearing & touch
Works by strengthening existing connections
& making new ones

May be possible to reduce brain damage by
blocking neural degeneration
 Apoptosis inhibitor proteins
 Nerve growth factor
 Estrogren
▪ Potentially explains why several brain disorders are less
common in women

Molecules that limit degeneration also
promote regeneration



Regeneration in mammalian CNS doesn’t
normally happen, but in the lab it can be induced
Potential treatment with transplantation of fetal
tissue into the brain or injection of embryonic
stem cells
Rehabilitation training can help by encouraging
brain reorganization
 Ex: treadmill for spinal cord injuries

Physically & mentally active individuals are less
likely to contract neurological disorders & if they
do, their symptoms are more mild & they have
fuller recovery