Nervous system disorders Flashcards
causes for learning and developmental disabilities
genetic
nutritional
infections
toxic exposures
perinatal complications (premature birth, birth asphyxia)
injury (brain injury, child abuse/neglect)
Poverty, economic retardation
Alzheimers disease
Most common form of dementia: deterioration of intellectual AND cognitive skills
Characterised by deposition of amyloid protein and disruption of neuronal cytoskeleton
three main cytoskeleton polymers
microtubule
neurofilament
microfilament
pathology of alzheimers
Abnormal build up of proteins in & around brain cells
Intracellular: abnormal association of TAU proteins (due to it being misfolded) with the microtubule leads to the microtubule disintegrating (TAU stabilises) and TAU forming clumps (neurofibrillary tangles)
Extracellular: plaques caused by build up of abnormally configured amyloid protein
** may be link between these: amyloid may cause neurons to produce abnormal TAU which then causes cell death
Distribution of these plaques is uneven but cause is unknown
Epilepsy
Characterised by two or more unprovoked seizures
Seizure = transient, hyper-synchronous abnormal neural activity
treatment for epilepsy
GABA agonsits -> increases inhibition which helps to prevent synchronisation
Categories of epilepsy
- idiopathic: genetic basis (genes effecting neuronal excitability)
- secondary/symptomatic: cause by know CNS injury or disorder
- cryptogenic: no clear etiological factor
Multiple sclerosis
Chronic auto-immune disease against myelin in CNS, 2:1 ratio females:males effected
Causes variety of symptoms that appear & disappear (spots of inflammation can be seen on t2 weighted MRI)
Nerves near ventricles are higher risk -> often vision is affected first
Schizophrenia symptoms
Prodromal signs: Negative symptoms (loss of function) including
Social withdrawal, neglect of personal hygiene, odd behaviour, flattened affect & paucity of speech
Non-psychotic signs:
Become overloaded w info, difficulty in crowded rooms, easily distracted, periods of great mental activity/excitement/creativity
Psychotic episodes: hallucinations & delusions
-> misattributions of significance (salience), prefrontal cortex
Dopamine hypothesis of schizophrenia
D2 receptor antagonists are effective in treating schizophrenia -> does dopamine overactivity cause schizophrenia?
Problems:
1. dopamine antagonists bind quickly but symptom relief takes several weeks
2. some drugs cause psychotic states similar to schizophrenia do not act on dopamine receptors (eg angel dust/PCP acts on glutamate receptors)
3. some people with schizophrenia don’t respond to D2 agonists but to drugs with broad monoamine antagonism
brain areas involved in depression
Increased activity has been observed (via fMRI) in:
Amygdala (fear)
Orbital & medial prefrontal cortex (bad thoughts)
Mediodorsal nucleus of the thalamus (association inputs to the prefrontal cortex)
The abnormally high blood disappears when depression is resolved regardless of treatments (or lack of)
** however this is not true for all areas of depression, now being questioned
Treatments for depression
- electroconvulsive therapy (recent memory is lots but can be very effective)
- psychotherapy
- antidepressants
Types of anitdepressants
Monoamine reuptake inhibitors: SSRIs/NERIs, tricyclics
MAO inhibitors: inhibit enzymatic breakdown of monoamines
Lithium: mechanism unknown
Monoamine hypothesis debate
Slow onset effect: hard to explain
Largely distributed targets (overall “state” of brain?)
Placebo effect: antidepressants can work but there is increasing evidence for a large placebo effect and little evidence for long-term efficacy
Serotonin hypothesis very questionable
mechanism of alcohol
Unknown exact mechanism, both stimulant and depressant:
1. binds to GABA receptors, both potentiate and antagonises GABAs effects
- interfere with glutamate action -> glutamate receptor sites in hippocampus (memory)
- stimulates release of serotonin and endorphins
- increases release of dopamine
