1. March 20, 2013

2.  Brain Tumors  Cerebrovascular Disorders (Strokes)  Cerebral Hemorrhage & Ischemia  Closed-Head Injuries  Infections  Bacterial & Viral  Neurotoxins  Genetic Factors  Programmed Cell Death

3.  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

4.  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

5.  Epilepsy  Parkinson’s Disease  Huntington’s Disease  Multiple Sclerosis  Alzheimer’s Disease

6.  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

7.  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

8.  2 types 1. Partial  Partial seizure does not involve the whole brain  Caused by synchronous burst of neuron firing 2. Generalized  Entire brain is involved  Grand mal (“classic” seizure)  Petit mal (no convulsions)

9.  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

10.  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

11.  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

12.  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

13.  Neuroplastic responses to brain damage 1. Degeneration 2. Regeneration 3. Reorganization 4. Recovery of function

14.  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 2. Retrograde degeneration  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

15.  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

16.  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

17.  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

18.  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