Alterations of Neurological functioning Flashcards

1
Q

The three types of dementia

A
  • Alzheimer’s
  • Multiple Sclerosis
  • Parkinson’s disease
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2
Q

Dementia overview

A

Progressive deterioration of cerebral function including a decline in orientation, memory, language, executive attention functioning and behavioral alterations

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3
Q

Dementia causes

A

-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

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4
Q

Alzheimer disease overview

A

*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
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5
Q

Types of Alzheimers

A
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
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6
Q

Risk factors for late onset AD

A

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

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7
Q

Alzheimer’s protective factors

A

-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)

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8
Q

Alzheimer’s pathophysiology

A

*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
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9
Q

Alzheimer’s early signs clinical manifestations

A

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

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10
Q

Alzheimer’s later signs clinical manifestations

A

-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

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11
Q

Parkinsons overview

A

A complex motor disorder caused by neurodegeneration in the basal ganglia. 2nd most common

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12
Q

Parkinson’s causes

A

-Idopathic
..most common; unknown cause

-Genertic
..autosomal dominant and recessive traits have been identified

-Gene- environment interaction

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13
Q

Parkinson’s Risk Factors

A

-age

-positive family history
…12-14x more likely with family

-Male gender

-Race
..white > blacks

-TBI

-Environmental exposure
…Herbicide and pesticide, metals, well water

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14
Q

Parkinson’s Patho

A
  • 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
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15
Q

Normal role of dopamine

A

-Fine tuned coordination and movement

-Acetylcholine works in conjunction with dopamine to produce smooth movement
….lack of dopamine causes tremors

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16
Q

Clinical consequences of Parkinson’s

A

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

17
Q

Multiple Sclerosis overview

A
  • 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
18
Q

Causes of Multiple Sclerosis

A

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
19
Q

Myelin sheath function

A
  • formed from glial cells (oligodendrocytes in the CNS)

- main function is to speed up the conduction of the nervous system impulse

20
Q

Multiple Sclerosis patho

A

*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

21
Q

Multiple Sclerosis clinical consequences

A

-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)