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Week 3- Multiple Sclerosis, PD, AD
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Materials
Lecture
Week 3.pptx
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Multiple Sclerosis
Chronic, progressive, degenerative
Disorders of the CNS characterized by demyelination of nerve fibers of the
Brain
Cranial Nerves (Optic Nerve)
Spinal Cord
Different types of MS
Loss of myelin interferes with conduction of impulses in affected fibers
May affects motor, sensory, & autonomic fibers
Occurs in diffuse patches in the nervous system
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MS Characteristics
Remissions & exacerbations but eventually progressive degeneration
Impairs cognitive function, especially attention to tasks & memory
Multiple Sclerosis Etiology
Idiopathic
Possibly related to:
Infections
Immune system
Genetic Factors (European descent, close relatives)
Environmental factors (climate)
Multiple Sclerosis
Onset usually between ages 20-40
A peak at 30 years
Women > or < men? Ratio?
2:1
Higher if European descent
Increased risk for close relatives
Canada has one of the highest rates in the world (prevalence 100,000)
More common in temperate climate
Multiple Sclerosis Pathophysiology
Lesions occur as a result of an inflammatory response as cells that do not normally enter the
brain & spinal cord do so & attack the neuron
Result in the loss of the protective myelin sheath in the white matter of the brain & SC
Often considered an autoimmune disease
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Multiple Sclerosis Pathophysiology
Chronic inflammation & demyelination of nerve fibers with scar formation in the CNS
Without myelin, nerve impulses slow down. Once axons are destroyed, impulses are totally
blocked
Results in permanent loss of nerve function
Affects all types of nerve fibers
Pathogenesis of MS
Multiple Sclerosis Pathophysiology
Scar tissue causes plaque formation
Plaques are scattered throughout the CNS
Eventually visible on MRI
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https://www.youtube.com/watch?v=K8R5N7ZMl
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Multiple Sclerosis Clinical Manifestations
Vague symptoms occur intermittently over months & years
Varies with individual
MS may not be diagnosed until long after the onset of the first symptom
Multiple Sclerosis: Clinical Manifestations
Characterized by:
Chronic, progressive deterioration in some
Reissions & exacerbations in others
Common signs & Symptoms include:
Motor
Sensory
Cerebellar
Emotional Changes
Multiple Sclerosis Clinical Manifestations
Early
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Blurred vision, weakness in legs
Diplopia, scotoma, dysarthria if CN’s affected
Paresthesia- numbness, burning, tingling
Progressively: Weakness & paralysis of limbs, trunk & head
Loss of coordination, bladder, bowel, sexual dysfunction
Spasticity of muscles
Later: Depression or euphoria
Additional Sensory Manifestations
Vertigo & tinnitus
Decreased hearing
Chronic neuropathic pain
MS: Clinical Manifestations
Cerebellar Manifestations *Match the terms*
Dysarthria
Lack of coordination in articulating speech
Dysphagia
Difficulty swallowing
Nystagmus
Involuntary horizontal eye movements
Ataxia
Lack of voluntary coordination of muscle movements that includes
gait abnormality
MS: Other Clinical Manifestations
Bowel & Bladder Functions
Constipation
Spastic bladder: small capacity for urine results in incontinence
Flaccid bladder: large capacity for urine and no sensation to urinate
Sexual dysfunction
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Erectile dysfunction
Decreased libido
Difficulty with orgasmic response
painful intercourse
Decreased lubrication
Major Types of Types of Multiple Sclerosis
Relapsing-remitting
Secondary progressive
Progressive-relapsing
Primary progressive
Types of MS
Relapsing-Remitting MS
Acute episodes
Recovery & stable course between relapses
85% of cases
Secondary-Progressive MS
Begins with a relapsing-remitting course
Later becomes steadily progressive
Relapses & partial recoveries may occur
Primary-Progressive MS
Steady & gradual neurologic deterioration
NO remission of symptoms
Progressive disability with no acute attacks
10% of cases
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Progressive Relapsing MS
Follows a progressive course from onset
Punctuated by relapses
Significant recovery immediately following relapse
Between relapses there is gradual worsening of symptoms
Multiple Sclerosis Diagnostic Studies
Based primarily on:
Patient history
Clinical manifestations
Ruling out other causes of symptoms
No definitive diagnostic test
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MRI- demonstrates presence of plaques
May have elevated protein, gamma globulin & lymphocytes levels in CSF
Parkinson’s Disease
Etiology
Primary Idiopathic
Genetic/ environmental factors
Secondary Parkinsonism caused by:
Encephalitis
Trauma
Vascular Disease
Drug-induced (ex. phenothiazine tranquilizers)
Parkinson’s Disease
Progressive Degenerative disorder of the CNS
Decrease in dopamine production
Typically over the age of 60 years
Mainly affects the motor system
Symptoms appear slowly over time
Males > females
Parkinson’s Disease Pathophysiology
The basal ganglia is located deep in the brain
This complex structure is responsible for voluntary motor control with neurotransmitters
The neurotransmitters that balance & refine voluntary motor movement are Dopamine &
Acetylcholine
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Dopamine & Acetylcholine are produce in the neurons located in the substantia nigra, a part
of the basal ganglia
Decrease in the number of numbers secreting the inhibitory neurotransmitter
dopamine
Leads to an imbalance between excitation & inhibition
Parkinson’s Disease: Pathophysiology
The neurons are damaged & do not produce enough Dopamine
Dopamine: Inhibitory (slows things down)
Acetylcholine: Excitatory (speeds things up)
80% or more of dopamine-producing cells lost by the time symptoms appear
https://www.osmosis.org/learn/Parkin
son_disease
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Parkinson’s Disease Clinical Manifestations
Early Signs & Symptoms
Fatigue
Muscle weakness & aching
Decreased flexibility
Less spontaneous changes in facial expression (mask)
Tremors in the hands at rest, repetitive pill-rolling motions of hands
Later signs & Symptoms
Tremors affect hands, feet, face, tongue
Increased muscle rigidity
Difficulty initiating movements
Slow movements (bradykinesia)
Characteristic standing posture is stooped, leaning forward with shuffling gait
Complex activities become slow and difficult.
Cardinal Signs: TRAP
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Parkinson’s Disease
Other Functions affected
Low voice, no infection
(hypophonia)
Dysarthria
Difficulty sleeping
Chewing & swallowing become
difficult
Prolonging eating time
Recurrent drooling
–Face might resemble a mask
Blinking of eyelids reduced
Blank, staring face
Manifestations
Urinary Problems or Constipation
Improper functioning of ANS (regulates smooth muscle)
Incontinent or trouble urinating.
Constipation gut slows, poor diet, drinking too little fluid, medications
Skin Problems
Face very oily, dandruff, or very dry, +++diaphoresis.
Seborrhoea (red, itchy, rash and white scales)
Sleep Problems
Difficulty staying asleep at night, restless sleep, nightmares & emotional dreams
Drowsiness or sudden sleep onset during the day
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Parkinson’s Disease
Other functions affected
Autonomic dysfunction
Urinary retention
Constipation
Orthostatic hypotension
Increased risk of falls
Urinary tract & respiratory tract infections are common complications
Dementia develops late in course of disease
Dementia
Progressive Chronic Disease
Cortical function is decreased.
Impaired cognitive skills
Impaired thinking, judgment, and learning
Memory loss
Confusion
Behavioural and personality changes
Many Causes of Dementia
Vascular disease
Infections
Genetic disorders
Dementia in Canada
45% greater risk if you smoke
65% of those dx over age 65 are women
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16,000 of those with dementia < 65 years old
Incidence 25,000
Prevalence 564,000 (56,000 are being cared for in hospital-ALC)
1.1 million people affected directly or indirectly (caregivers)
Prevalence anticipated to be 937,000 within 15 years
Pathophysiology: AD
Progressive Cortical Atrophy
Neurofibrillary tangles and senile plaques
ACH deficit caused by loss of neurons
No Definite diagnostic tests available
Exclusion of other disorders
Careful medical and psychological history
Progressive tests of memory important (MMSE)
Specific Cause Unknown
Repetitive DNA sequences on different chromosomes have been associated with AD.
Depending on defective genes, may have early (before age 65) or late onset
Pathological Changes with Alzheimer’s Disease
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Figure 14-32, B—Alzheimer’s disease.
Brain is smaller, with narrower gyri and
wider sulci.
Figure 14-32, C—normal brain.
Clinical Manifestations Alzheimer’s Disease (AD)
Extend over 10-20 years
Gradual loss of memory & lack of concentration
Decline of cognitive function
Behavioural Changes
Irritability, hostility, mood swings
Impaired learning, poor judgement
Changes in food intake
Inability to recognize family, lack of environmental awareness, incontinence, inability to
function
Other Forms of Dementia
Vascular dementia
Caused by cerebrovascular disease
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Often a result of multiple small brain infarctions
Common in persons older than 70 years
Especially in those with hypertension
Onset insidious
Memory loss, apathy, inability to manage daily routines
Progression may be in stages.
Other neurologic impairment is common.
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