BRAIN TRAUMA DP9 Flashcards
Brain trauma
Any brain injury acquired after birth that impairs normal functioning
- mild / severe
- temporary / permanent
- congenital (inherited) but most are acquired through life events after birth (eg. stroke, infection, lack of oxygen, drugs, tumour, neurodegenerative disease)
Neurodegenerative Disease
A disorder characterised by the progressive decline in the structure, activity and function of the brain tissue
- Groups of neurons in the brain gradually become damaged/deteriorate and lose their function
- The gradual decrease is usually age related
Eg: Parkinson’s disease and
Dementia/alzheimers
Alzheimer’s disease
Is a neurodegenerative disease (type of dementia) that results from a loss of neurons in the hippocampus and causes memory loss, personality change and deterioration of cognitive and social skills.
Alzheimer’s disease
Differences in patients:
Rate of progression/symptoms vary from patients
Alzheimer’s disease
Diagnosis:
Difficult to diagnose as there is not one reliable/common symptom
Entirely accurate diagnosis can only be made after death with an autopsy and assessment of brain deterioration
Alzheimer’s disease Patients / medication
- use of medications to boost the ACh in the brain in early/middle stages of the disease can slow development of primary symptoms.
- Medications can improve efficiency of damaged neurons
- Medication can ease some secondary symptoms such as depression of alzheimers
Alzheimer’s disease cause
- High levels of abnormal structures that interfere with neural communication within and between neurons impairing normal brain function.
- Involve plaques and tangles that prevent essential nutrients traveling between neurons in the brain .
- Are buildups of protein that occur as part of normal ageing, but in people with Alzheimer’s, the amount of these proteins that build up are far greater
Neurotransmitter acetylcholine (ACh). Cortical shrinkage of the cerebral cortex
Amyloid plaques (protein deposits)
Amyloid plaques are fragments of protein that build up around the outside of neurons
Neurofibrillary tangle
Neurofibrillary tangles are caused by tau protein deposits inside neurons that inhibit the cells ability to transport nutrients.
Neurotransmitter acetylcholine (ACh).
Build up amyloid and tau may contribute by destroying the neurotransmitter ACh and has a lower supply. Therefore it must be important for learning and memory
Cortical shrinkage of the cerebral cortex
When neurons die due to neurofibrillary tangles and amyloid plaque building up in the brain, causing the brain to shrink.
Alzheimer’s disease
Neurological symptoms:
- Very large air pockets in the brain
- Widespread death of neurons (as the brain cells die the brain shrinks) - neural tissue contains fewer neurons and synapses than a healthy brain
- Absence of brain matter to support memory function or recall, results in deterioration of LTM
- The medial temporal lobe is most significantly affected, particularly the hippocampus
Alzheimer’s disease Immediate behaviour symptoms
- Starts slowly - symptoms are subtle, person can function with minimal assistance
- Unusual irritability, impaired decision making
- Reduced interest in hobbies and social activities (continues + becomes LT symptoms as well)
Alzheimer’s disease
Long term behaviour symptoms
- Memory loss, especially declarative (explicit) memories (unable to recognize fam)
- Personality change (impacted by frontal lobe - cortical shrinkage results in less capacity to control our personality)
- Confusion and disorientation (debilitating disorder), repetition in behaviour
- Includes memory loss of: significant events, words, names, directions, inability to follow a story, everyday skills (dressing, cooking..)
Amnesia
Refers to a loss of memory that is inconsistent with ordinary forgetting, and may be temporary or permanent, partial or incomplete
General symptoms include:
- Difficulty with certain types of info (eg. explicit but not implicit)
- Debilitating and distressing
- Implicit (procedural and conditioned responses) memories aren’t affected
Anterograde amnesia
A = after
An inability to form new memories after brain damage
→ often long term
→ less likely to recover
Retrograde amnesia
An inability to retrieve previously stored memories after brain damage
→ often short term
→ previously stored memories are there but difficult to access (usually comes back over time w/ triggers)
Difference in symptoms
Anterograde amnesia
→ can no longer encode (form or store) new LTM due to disruption to consolidation
→ nothing new can get from STM to LTM
→ little difficulty retrieving what has happened since the injury
Retrograde amnesia
→ no longer retrieve previously stored LTM
→ can still encode new LTM through consolidation
→ episodic memory is more severely affected than semantic
Biological cause of different amnesia
check w wolters
Anterograde amnesia
→ damage hippocampus (unable to encode explicit memories)
Retrograde amnesia
→ damage to cerebral cortex (unable to process STM)
Physical cause, likelihood
Anterograde amnesia
→ drugs, traumatic brain injury: when the brain is struck hard, it slams against the inside of the skull, causing brain tissue to tear, twist or bleed
→ less common
Retrograde amnesia
→ due to head trauma or accident. car accident: causes a jolt to the head which jolts the brain too
→ more common
Brain surgery Hippocampus
Inability to form new LT explicit memories
- Inability to transfer memories from STM to LTM (impaired consolidation)
- can’t remember new details
Brain surgery Cerebellum
Impaired procedural and classically conditioned memory formation (will still remember the learning process, but will not form a classically conditioned motor response)
Brain surgery Cerebral cortex
Can’t remember past personal details
- Serious memory impairments
Brain surgery Amygdala
Unable to acquire a conditioned fear response
- Impaired formation of emotional memories
