Alterations of Neurological functioning Flashcards
The three types of dementia
- Alzheimer’s
- Multiple Sclerosis
- Parkinson’s disease
Dementia overview
Progressive deterioration of cerebral function including a decline in orientation, memory, language, executive attention functioning and behavioral alterations
Dementia causes
-Ischemia
…cardiovascular disease leads to ischemia of CNS neurons and neuronal dysfunction and degeneration
> not enough blood flow to brain, seeing atrophy/ death of neurons
-Dementia with Lewy bodies (DLB)
..accumulation of proteins within neuron cytoplasm disrupts synaptic function
>protein in the neural system does not allow synapses to be fired
-Alzheimer Disease
..most common cause of dementia
Alzheimer disease overview
*Dementia characterized by progressive failure of cerebral function not associated with an impaired level on consciousness
Mental impairments include ;
- oritentation
- recent memory
- remote memory
- language
- executive attentional function
- behavior
Types of Alzheimers
EARLY ONSET (rare) -Occurs in people age 30-60
- accounts for < 5% of AD cases
- caused by single-gene mutations that cause abnormal proteins to be formed (genetic mutation causes alz)
LATE ONSET (most common) -Develops after age 60
- Most common form of AD
- Combinations of genetic susceptibility, environment and immunoglobulin factors
Risk factors for late onset AD
NON MODIFIABLE
-age
..older you get the higher is your risk
-Family history/genetics
..mutation increase by 3-8x with family members
- Sex; Female > males
- Race/Ethnicity; Blacks, Hispanics > whites
MODIFIABLE
-Cardiovascular disease (and risk factors including hypertension, smoking and obesiety)
….ischemia cause more progressed dementia
-Social and cognitive engagement
..higher rate in less socially active people
-Traumatic brain injury (TBI)
..concussions, chronic traumatic encephalopathy
>Brain shrinks in atrophy during TBI
Alzheimer’s protective factors
-Physical Activity
-antioxidants
..free radicals can cause brain injury)
-low calorie diet
-drugs;
..statins (lipid lowering medication) and non-steroid anti-inflammatory drugs (NSAIDs) (ibeuprophen)
Alzheimer’s pathophysiology
*characterized by the accumulation of amyloid plaques and neurofibrillary tangles spread through the brain causing neuronal dysfunction and cell death
AMYLOID PLAQUES
-accumulation of amyloid beta peptides in the extracellular matrix surrounding the CNS neurons
-Amyloid beta peptides form clusters that block neurotransmitter release and cause cell injury
…..accumulate {outside} of neurons
NEUROFIBRILLARY TANGLES
-Caused by the deposits of tau proteins that accumulate in the cytoplasm of the neurons
….accumulate {inside} the neuron
- In AD, tau protein accumulates inside the cells and destory the microtubule system, therefore nutrients and other molecules are unable to move throughout the cell
- Leads to cell death
Alzheimer’s early signs clinical manifestations
EARLY SIGNS
-Alzheimer disease starts with 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 disinhibited during these episodes
Alzheimer’s later signs clinical manifestations
-Cognitive Decline
..in addition to short/long term memory loss– decline in decision making, speech and language (asphasia) and recognition abilities
-Mood disturbances
..irritability, depression,anxiety, tendency of violent outbursts
-Motor changes
… if the disease affects the frontal lobe, motor problems such as muscle rigidity, flexion posturing and propulsion/repulsion are common. eventually unable to walk
-Function decline
..bowel and urinary incontinence
Parkinsons overview
A complex motor disorder caused by neurodegeneration in the basal ganglia. 2nd most common
Parkinson’s causes
-Idopathic
..most common; unknown cause
-Genertic
..autosomal dominant and recessive traits have been identified
-Gene- environment interaction
Parkinson’s Risk Factors
-age
-positive family history
…12-14x more likely with family
-Male gender
-Race
..white > blacks
-TBI
-Environmental exposure
…Herbicide and pesticide, metals, well water
Parkinson’s Patho
- disorder of sequential progression: motor function changes in early stages progressing to cognitive and psychological changes in alter stages
- Degeneration neurons that release dopamine in the substantia ganglia of the basal ganglia
CAUSES of decreased dopamine;
-free-radical injury
- toxins; external or internal toxins destroy dopamine producing neurons
- Age-related changes- normal age related reduction of dopamine producing cells is accelerated
Normal role of dopamine
-Fine tuned coordination and movement
-Acetylcholine works in conjunction with dopamine to produce smooth movement
….lack of dopamine causes tremors
Clinical consequences of Parkinson’s
ABNORMAL MOTOR MOVEMENTS
-Resting tremor
…asymmetric at first and most evident in one hand at rest
-Muscle Rigidity
>Muscle tone increased in both flexor and extensor muscles providing a constant resistance to passive movements of the joints
> cogwheel rigidity; brief jerks, with tremor
-Bradykinesia
..slowness of movements and difficulty with ADL’s
-Posture instability
>postural fixation with PD is involuntary flexion of neck/head
>balance and rigidity abnormalities are common
DYSFUNCTION OF THE AUTONOMIC NERVOUS SYSTEM
>impaired gastrointestinal motility
>bladder dysfunction
>orthostatic hypotension (low bp)
DEPRESSION
..Mild to moderate depression due to low dopamine
COGNITIVE IMPAIRMENT
..Mild cognitive decline including impaired visual-spatial perception, slowness in execution of motor tasks, and impaired attention/concentration
Multiple Sclerosis overview
- An autoimmune demyelinating disorder resulting in damage to the myelin sheath of CNS system
- age of onset 20-40 ..young
- females > males (2;1)
- Caucasians > other races
- Disease course can last > 30 years .. slow onset
Causes of Multiple Sclerosis
GENETIC RISK FACTORS
-Pattern of inheritance is unclear; > 50 genetic loci associated with increase susceptibility mutations in the genes that code for HLA (self vs nonself)
-Interleukin receptor mutations
…WBC used to communicate with each other
ENVIRONMENTAL RISK FACTORS
-Vitamin D deficiency/lack of UV exposure- more cases at higher latitudes
- Epsteen bar virus (EBV) infection
- Cigarette smoking
Myelin sheath function
- formed from glial cells (oligodendrocytes in the CNS)
- main function is to speed up the conduction of the nervous system impulse
Multiple Sclerosis patho
*Characterized by degeneration of the myelin sheath of CNS neurons, leading to inflammation , scarring, and loss of axons
AUTOIMMUNE DESTRUCTION OF MYELIN
-activation of Tc cells that damage, then cross blood brain barrier and target oligodendrocytes (glial cells that from the myelin) in the CNS
[Tc cells destroy myelin with toxins]
-Activation of B lymphocytes that produce autoantibodies that damage the myelin sheath (attacks your own tissue)
INFLAMMATION
-infiltration by neutrophil, macrophages and eosinophils; activation of complement proteins (phoagocytosis of myelin sheath bc of autoantibodies)
- phagocytes release of oxygen free radicals and glutamate ( a neurotoxin)
- Scarring and formation of ‘plaques’ (characteristic brain lesions in MS)
CONSEQUENCES OF DEMYELINATION
-Slowing down and halting nervous impulse transmission
-disruption of ion channels in neuromal membranes
AXON DESTRUCTION
Multiple Sclerosis clinical consequences
-Sensory loss and paresthesias (numbness and tingling)
-Motor Consequences
..muscle cramping, muscle weakness and muscle twitching
-Autonomic consequences
..bowel, bladder and sexual dysfunction
-Cerebellar dysfunction
..coordinating muscles (balance, gait, etc)
