Alterations Of Neuron Functions Flashcards
Dementia
Progressive determination of cerebral function including a decline in orientation, memory, language, executive attentional functioning and behavior alterations
Ischemia (dementia)
Cardiovascular disease leads to ischemia of CNS neurons and neuronal dysfunction and degeneration
Dementia with levy bodies (dementia)
Accumulation of proteins within neuron cytoplasm disrupts synaptic function
Alzheimer disease (dementia)
Dementia characterized by progressive failure of cerebral function not associated with an impaired level of consciousness
Mental impairments of (AD)
Orientation Recent memory Remote memory language Executive attention all function behavior
Early onset (rare) (AD)
Occurs in people age 30-60
Accounts for <5% of AD cases
Caused by single-gene mutations that cause abnormal proteins to be formed
Late onset (most commmon) (AD)
Develops after age 60
Most common form of AD
Combination of genetic susceptibility, environment and immunological factors
Non-modifiable (AD)
Age
Family history/genetics
Females mainly
Blacks, hispanics mainly
Modifiable (AD)
Cardiovascular disease
Social and cognitive engagement
Traumatic brain injury
Moderate TBI (AD)
Increases risk of dementia by 2.3
Severe TBI (AD)
increase risk of dementia by 4.5
Protective factors (AD)
Physical activity
Antioxidants
Low calorie diet
Statins and NSAIDs (ibuprofen)
Pathophysiology (AD)
Characterized by the accumulation of amyloid plagues and neurofibrillary tangles spread by the brain causing neuronal dysfunction and cell death
Amyloid plagues (AD)
Accumulation of amyloid beta peptides in the extracellular matrix surrounding the CNS neurons- accumulation are called amyloid plaques
Form clusters that block neurotransmitter release and also cause cell injury
Neurofibrillary tangles (AD)
Caused by deposits of tau protein that accumulate in the cytoplasm of the neurons
Tau protein (AD)
Accumulates inside the cells and destroy the microtubule system, therefore nutrients and other molecules are unable to move throughout the cell
Leads to cell death
Clinical manifestations Early signs (AD)
Alzheimer disease starts with a gradual onset of vague problems such as forgetfulness, emotional upset and fatigue
Short term memory becomes progressively worse and the individual often becomes disoriented or disinhibition during these episodes
Clinical manifestations Later signs (AD)
Cognitive decline
Mood disturbances
Motor changes
Function decline
Cognitive decline (AD)
In addition to the progressive of short and eventually long term memory, alzheimer disease causes a wide variety of other cognitive changes
Mood disturbances (AD)
AD leads to many mood disturbances including irritability, depression, anxiety.
Motor changes (AD)
If the disease process affects the frontal lobe, motor problems such as muscle rigidity, flexion posturing, propulsion, and repulsion are common
Function decline (AD)
Later stages of alzheimer disease present with bowel and urinary incontinence
Parkinson’s Disease
A complex motor disorder caused by neurological in the basal ganglia. 2nd most common neurodegenerative disease
Causes (PD)
Idiopathic
Genetic
Gene
Idiopathic (PD)
Most common
Genetic (PD)
Autosomal dominant and recessive traits have been identified
Gene (PD)
environment interaction
Risk factors (PD)
Age, family history, male, environmental exposure, whites mainly, traumatic brain injury
Pathophysiology (PD)
Disorder of sequential progression
Degeneration neurons that release dopamine in the substantial Nigeria of the basal ganglia
Degeneration neurons released caused by (PD)
Free-radical injury
Toxins
Age related changes
Normal role of dopamine (PD)
Fine-tune coordination of movement
Acetylcholine works in conjunction with dopamine to produce smooth movement
Progressive loss of dopamine (PD)
Activity and relative excess of acetylcholine activity in the basal ganglia leads to loss of smooth motor movements and other changes
Clinical consequences
Abnormal motor movements (PD)
Resting tremor
Muscle rigidity
Bradykinesia
Postural instability
Resting tremor (PD)
Usually asymmetric at first and most evident in one hand
Muscle rigidity (PD)
Muscle tone increased in both flexor and extensor muscles providing a constant resistance to passive movements of the joints
Bradykinesia (PD)
Generalized slowness of movement and difficulty with ADL’s
Postural instability (PD)
Postural fixation with PD is involuntary flexion of neck and head
Balance and righting abnormalities common
Clinical consequences (PD) Dysfunction of the autonomic nervous system
Impaired gastrointestinal motility
Bladder dysfunction
Orthostatic hypotension
Clinical consequences (PD) Depression
Mild to moderate
Clinical consequences (PD) Cognitive impairment
Mild cognitive decline including impaired visual-spatial perception, slowness in execution of motor tasks
Multiple sclerosis
An auto immune demyelinating disorder resulting in damage to the yelping sheath of CNS neurons Age of onset is 20-40 years Females Caucasian s Lasts more that 30 years
Etiologies (MS)
Combinations of genetics and environment factors
Genetic risk factors for (MS)
Pattern of inheritance is unclear
Over 50 genetic loci
Interleukin receptor mutations
Environmental risk factors (MS)
Vitamin D deficiency
EBV infection
Cigarette smoking
Myelin sheath structure and function
Formed from glial cells
Main function is to speed up the conduction of the nervous impulse
Pathophysiology (MS)
Characterized by degeneration of the myelin sheath of CNS neurons, leading to inflammation, scarring, and loss of axons
Autoimmune destruction of myelin (MS)
Activation of Tc cells, cross blood barrier to attack oligodendrocytes (glial cells forming myelin) in the CNS
Activation of B lymphocytes that produce antibodies that damage myelin sheath
Inflammation (MS)
Infiltration by neutrophil, macrophages and eosinophils
Phagocytes release of oxygen free radicals and glutamate
Scarring and formations of plaques
Consequences of demyelination (MS)
Slowing down and halting of nervous impulse transmission
Disruption of ion channels in neuronal membranes
Axonal destruction (MS)
Firing of action potentials no longer if axons destructed
Clinical consequences (MS)
Sensory loss of paresthesias
Motor consequences
Autonomic consequences
Cerebellar dysfunction
