Chapter 10 - Chapter 10: Brain Damage and Neuroplasticity...

Info iconThis preview shows pages 1–3. Sign up to view the full content.

View Full Document Right Arrow Icon
Chapter 10: Brain Damage and Neuroplasticity The case of Prof. P Lets meet the man in person and listen to what he has to say. The case: was it hearing loss due to middle age or something a little more sinister? 10.1 Causes of Brain Damage Brain tumors Cerebrovascular disorders Closed-head injuries Infections of the brain Neurotoxins Genetic factors All the above can trigger apoptosis (programmed cell death) Brain Tumors A tumor (neoplasm) is a mass of cells that grows independently of the rest of the body – a cancer (can be benign or malignant) ~20% of brain tumors are meningiomas – encased in meninges - Encapsulated, growing within their own membranes - Usually benign (non-dangerous), surgically removable Most brain tumors are infiltrating - Grow diffusely through surrounding tissue - Malignant, difficult to remove or destroy About 10% of brain tumors are metastatic – they originate elsewhere, usually the lungs Cerebrovascular Disorders Stroke – a sudden-onset cerebrovascular event that causes brain damage - Cerebral hemorrhage – bleeding in the brain/blood vessel ruptures o Aneurysm – a weakened point in a blood vessel that makes a stroke more likely, may be congenital (present at birth) or due to poison or infection - Cerebral ischemia – disruption of blood supply o Thrombosis – a plug forms in the brain o Embolism – a plug forms elsewhere and moves to the brain o Arteriosclerosis – wall of blood vessels thicken, usually due to fat deposits 3 rd leading cause of death in the U.S. and most common cause of adult disability
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full DocumentRight Arrow Icon
Damage due to Cerebral Ischemia Does not develop immediately Most damage is a consequence of excess neurotransmitter release – especially glutamate Blood-deprived neurons become overactive and release glutamate to adjacent neurons Glutamate over-activates its receptors, especially NMDA receptors leading to an influx of Na + and Ca 2+ Influx of Na + and Ca 2+ triggers - The release of still more glutamate - A sequence of internal reactions that ultimately kill the neuron Ischemia-induced brain damage - Takes time - Does not occur equally in all parts of the brain - Mechanisms of damage vary with the brain structure affected Figure 10.5 – Stroke-induced release of glutamate Aneurysms: Closed-Head Injuries Brain injuries due to blows that do not penetrate the skull – the brain collides with the skull - Contrecoup injuries – contusions are often on the side of the brain opposite to the blow Contusions – closed-head injuries that involve damage to the cerebral circulatory system; hematoma (bruise) forms Concussions – when there is disturbance of consciousness following a blow to the head and no evidence of structural damage - While there is no apparent brain damage with a single concussion, multiple concussions
Background image of page 2
Image of page 3
This is the end of the preview. Sign up to access the rest of the document.

Page1 / 12

Chapter 10 - Chapter 10: Brain Damage and Neuroplasticity...

This preview shows document pages 1 - 3. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online