CNS-unit 2

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Unit 2: CNS disorders• Lesson 1: Central Nervous System Disorders

Review of structure and function

• List the major vessels in the cerebral circulation and describe how the Circle of Willis was formed.

• Review the following topics:

– Limbic system

– Long term and short term memory

• Vascular Diseases

• Compare the major causes, pathophysiology and clinical features of different types of cerebrovascular accidents.

– Ischemic

– Hemorrhagic

• Intracerebral

• Subarachnoid

– Transient-ischemic attacks (TIAs)

• Discuss the various types of aneurysms including arterio-venous malformations (AVMs)• Discuss the risk factors, symptomatology, assessment of Glasgow coma scale and investigations done for stroke patients.

• Sequelae of stroke and brain injury

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• Describe the pathophysiology of cerebral edema.

• Describe increased intracranial pressure

– Common causes, Clinical Manifestations, and Prevention1

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Review of structure and function

• Primary functions – Frontal lobe

– Parietal lobe

– Temporal lobe – Occipital lobe

• Higher order functions

– Supplementary areas, association cortex – Limbic System

– Basal ganglion

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Higher Order Functions of the Frontal Lobe

• Abstract vs. concrete reasoning

• Motivation/volition

• Concentration

• Decision making• Purposeful behavior

• Memory, sequencing, making meaning of

language• Speech organization and production

• Aspects of emotional response

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Higher Order Functions of the Parietal Lobe

• Sensory integration and spatial relations

• Bodily awareness

• Filtration of background stimuli• Personality factors and symptom denial

• Memory and nonverbal memory

• Concept formation

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Higher Order Functions of the Temporal Lobe

• Visual-spatial recognition

• Attention

• Motivation• Emotional modulation and interpretation

• Impulse and aggression control

• Interpretation and meaning of socialcontact

• Aspects of sexual action and meaning

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Higher Order Functions of the Occipital lobe

• Meaningfulness of visual experience

• Depth perception

• Pattern, form and location in space

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• Supplementary motor area – preparatory

role in programming of complex

sequences

• Premotor cortex – assists primary motor

cortex

• Posterior parietal cortex – guides premotor

cortex

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Limbic System

• Includes portions of the hypothalamus and

other forebrain structures that encircle

brain stem

• Responsible for

– Emotion

– Mood (happiness, anger, fear)

– Plays important role in motivation and

learning

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Frontal lobe

Cingulate gyrus

Fornix

Thalamus

Hippocampus

Temporal lobe

Amygdala

Hypothalamus

Olfactory bulb

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Memory

• Storage of acquired knowledge for later recall• Memory trace

– Neural change responsible for retention or storage ofknowledge

• Short-term memory – Lasts for seconds to hours

• Long-term memory – Retained for days to years

• Consolidation – Process of transferring and fixing short-term memory

traces into long-term memory stores

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• storage in 2 stages

• short-term memory

long-term memory

consolidation

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Newly acquired

information

Usually

permanently lost Rapid retrieval

Inability to

retrieve“Forgetting” “Remembering”

Searching and

readout

Short-term

memory stores

(Practice)

Consolidation

Long-termmemory stores Slower retrieval, except for

thoroughly ingrained memories,

which are rapidly retrieved

Usually only

transiently unable

to access stores

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Integration of thought, mood, learning,

and cognition

• learning and memory

behavior

through environment, social, culture

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• Psychiatric or brain injured patients

difficulty in learning and memory

impact on behavior and

the design of effective intervention

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Vascular Diseases

• Abnormalities of cerebral perfusion

causing strokes/cerebrovascular accidents

(CVA)

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CVA (cerebrovascular accidents)/stroke

• a clinical syndrome characterized by a

focal neurological deficit, due to an

abnormality of the cerebral circulation

• review on cerebral circulation

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Blood Supply to the Brain

• Two internal carotid arteries anteriorly

– Ophthalmic, posterior communicating, anterior

choroidal, anterior cerebral, and middle

cerebral

• Vertebral arteries posteriorly

• Internal carotid and vertebral arteries

communicate at the base of the brainthrough the circle of Willis.

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Blood Supply to the Brain

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Etiology (risk factors)

• Age

• Gender

• Race

• High cholesterol levels

• Cigarette smoking

• Diabetes mellitus

• Other risk factors – Heart diseases

– Blood diseases – Alcohol, cocaine and illicit drug use (Chlamydia pneumoniae)

– Sedentary life style

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Classification of stroke

• According to pathophysiology:

– 1. ischemic stroke – due to thrombosis and/or embolism

– 2. hemorrhagic stroke – intracerebral hemorrhage

– subarachnoid hemorrhage

T o Main T pes of Strokes (Brain

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Two Main Types of Strokes (Brain

Attack)

• Ischemic strokes – Caused by an interruption of blood flow in a

cerebral vessel and are the most common type

of stroke, accounting for 70 –80% of all strokes.

– Caused by thrombosis and/or embolism

• Hemorrhagic strokes

– Caused by bleeding into brain tissue, usually

from a blood vessel rupture caused by

hypertension, aneurysms, arteriovenous

malformations, head injury, or blood dyscrasias

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What is thrombosis?

• a solid mass of blood constituents (blood

clot) formed within the vascular system in

a living being

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Predisposing factors for

thrombosis• Changes in the intimal surface of the blood

vessel

• Changes in the pattern of blood flow

• Changes in the blood constituents

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Embolism

• is a mass of material in the vascular

system able to become dislodged within a

vessel and block its lumen

– a piece of thrombus

– foreign bodies

– fat tissue

– bacterial organism

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• Hemorrhage

– severe hypertension – aneurysm

– congenital berry aneurysm

– arteriovenous malformation – bleeding disorders

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Cerebral Aneurysm

• Lesion of an artery that results in

dilation and ballooning of a segment

of the vessel

• High blood pressure, acute alcohol

intoxication, and recreational druguse (especially cocaine) implicated

• Congenital defect of the medial layer

of the artery weakens, allowingdilated portion to fill with blood and

eventually burst causing hemorrhage;

most found in circle of Willis

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Signs and Symptoms of

Cerebral Aneurysms• Most small aneurysms are asymptomatic.

• Large aneurysms may cause chronic

headache, neurologic deficits, or both.

• Other manifestations include signs ofmeningeal irritation, cranial nerve deficits,

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Arteriovenous malformation

• Capillary system fails to develop

appropriately with arterial blood shunted

directly into the venous system; causes

the vessels to progressively enlarge;becomes a congested mass of enlarged

vessels that can burst

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• blood is shunted from the high-pressure

arterial system to the low-pressure venous

system without the buffering advantage of

the capillary network. – The draining venous channels are exposed to

high levels of pressure, predisposing them to

rupture and hemorrhage.

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Bleeding disorders

• Platelet problems

– thrombocytopenia

• Clotting problems

– Hemophilia

• Leukemia

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Classification of stroke

• According to clinical condition

– TIA

– Evolving stroke (stroke in evolution)

– Completed stroke

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Pathophysiology

• destruction of brain substance

• edema of surrounding brain tissue

• increased intracranial pressure

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Clinical manifestations

• Determined:

– by the cerebral artery that is affected

– Size of the vessel – Lacunar infarct

– by the area of brain tissue that is supplied by

that vessel

– By the adequacy of the collateral circulation

– Presence or absence of cerebral edema andincreased ICP

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• anterior cerebral artery

• middle cerebral artery

• posterior cerebral artery

» Review page # 914, table 44- 2

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• What is the most common cause of

stroke?

• Why early treatment / intervention is

essential?

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Increased ICP

• Increased ICP can occur with space-

occupying lesions, vasogenic or cytotoxic

edema, or with obstruction or excessive

production of CSF

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Causes of Intracranial Pressure

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Increased Intracranial Pressure (IICP)

Whenever there is a rise in

intracranial pressure, the bodywill compensate first by

displacing the cerebrospinal

fluid to the spinal subarachnoidspace and increasedreabsorption of cerebrospinal

fluid.

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Increased intracranial pressure

• Brain is enclosed in the rigid confines of

the skull

• ICP can obstruct cerebral blood flow,

destroy brain cells, displace brain tissue

as in herniation and damage delicate brain

structures

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Types of Herniation

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consciousness

• is a state of awareness of self and the

environment and of being able to become

oriented to new stimuli

• rely on RAS (ascending fibers) for being

alert

• the content and cognitive aspects of

consciousness are determined by afunctioning cerebral cortex

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Levels of Consciousness

• Confusion – conscious but disorientated

• Delirium - restless, delusions

• Obtundation – decreased alertness with

psychomotor retardation

• Stupor – not unconscious, but no

spontaneous activity

• Coma - unarousable, unresponsive

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Level of Consciousness

• Change in level of consciousness (LOC)is most sensitive indicator of altered brain

function

• State of alertness and attentiveness toone’s environment and situation – Dependent on activity in the RAS neurons

• LOC may fluctuate; important to monitor

and treat changes• Complete loss of consciousness: coma

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Glasgow Coma Scale

• Standardized tool for assessing LOC inacutely brain-injured persons

• Numeric scores given to arousal-directed

responses of eye opening, verbalutterances, and motor reactions – Mild (>12), moderate (9 to 12), to severe (<8)

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Glasgow Coma Scale

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Glasgow Coma Score

Eye Opening (E) Verbal Response (V) Motor Response (M)

4=Spontaneous 5=Normal conversation 6=Normal

3=To voice 4=Disoriented

2=To pain conversation

1=None 3=Words, but not coherent

2=No words onlysounds

1=None

5=Localizes to pain

4=Withdraws to pain

* 3=Decorticate posture

* 2=Decerebrate posture1=None

* - see next slide for images

NOTE:

Severe brain injury = GCS ≤ 8Moderate brain injury = GCS 9 - 12

Minor brain injury = GCS ≥ 13

Lowest score = 3 (very poor prognosis)

Highest score = 15 (alert, oriented, no indications ofbrain injury)

Total Score = E+V+M

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Posturing

* A somewhat better

prognosis thandecerebrate posturingbecause the damage isnot as deep into the

brainstem.

* Poorer prognosisbecause the damage is

deeper into

the brainstem

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Investigations

• General

• Specific

– Chest X ray

– CT

– ?MRI

– ?arteriogram

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Nursing implications

• Nursing interventions

– Neurologic monitoring

– Cerebral edema management

– Seizure control

– Medication administration

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Lesson 2: Degenerative and immune related diseases

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Lesson 2: Degenerative and immune related diseases

• Degenerative Diseases

– Describe the types of dementia.

– Compare the etiology and clinical manifestations associated with:

• Alzheimer‘s Disease

– Causes, Pathophysiology, Clinical Manifestations

• Huntington‘s Disease

– Causes, Symptoms, Diagnosis, Prognosis – Explain the etiology, pathogenesis and clinical manifestations of

Parkinson disease.

• Genetic/immune related Diseases

– Discuss the etiology, pathophysiology and clinical manifestations

of Multiple Sclerosis (MS).

– Compare MS with ALS (Amyotrophic Lateral Sclerosis)

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Disorders of cognition• The term ―dementia‖ refers to a syndrome of cognitive impairment

• Caused by any disorder that damages large association areas of the cerebral cortex

or subcortical areas that serve memory and learning• Includes Alzheimer‘s disease, multi-infarct dementia, Pick‘s disease (Frontotemporal

Dementia), Wernicke-Korsakoff syndrome, and Huntington‘s Chorea

Dementia

• Dementia is the loss of mental functions—such as thinking, memory, and

reasoning—that is severe enough to interfere with a person‘s daily functioning.

• Dementia is not a disease itself, but rather a group of symptoms that might

accompany certain diseases or conditions.

• Symptoms also might include changes in personality, mood, and behavior.

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Dementia

• Syndrome associated with many pathologies;characterized by progressive deterioration and

continuing decline of memory and other cognitive

changes

• Impairment of short- and long-term memory,associated with abstract thinking, impaired

judgment, other higher cortical functions, orpersonality change

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Dementia

• Most common – Alzheimer

• Vascular – Results from single cerebrovascular insults

– Risk factors: stroke, hypertension, anddiabetes

Al h i ’ Di

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Alzheimer ’s Disease

• Alzheimer's Disease (AD) is a form of dementia, which is a medicalcondition that disrupts the way the brain works, causing progressive declinein intellectual functioning severe enough to interfere with a person's daily life

activities and social relationships.

• It is also sometimes called senile dementia of the Alzheimer type (SDAT).

• AD is defined by the presence of specific anatomic abnormalities in the

brain, called amyloid plaques and neurofibrillary tangles. These can only bedetected by direct examination of brain tissue, which means that

Alzheimer's disease is only diagnosed after death, via autopsy. In a livingperson, doctors diagnose "probable AD" if a person shows all the behavioralsymptoms of AD, and if all other possible causes of dementia are ruled out.

• AD accounts for more than 50% of all cases of dementia. The mostcommon form of Alzheimer's occurs in people older than 65 years, but thereis also a form called early-onset Alzheimer's disease or pre-senile dementiawhich can begin as early as age 40.

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Alzheimer‘s disease

• Etiology

– Aging, genetic linkage – mutations in

chromosome 21, 14 and 1

• Pathophysiology – degeneration of neurons in temporal and

frontal lobes, brain atrophy, amyloid plaques,

and neurofibrillary tangles

– Associated ventricular enlargement

– Deficient synthesis of brain acetylcholine

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• Pathological features

– Senile plaques and neurofibrillary tangles

– Amyloid beta derived from APP

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Pathological Changes in the Brain

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Pathological Changes in the Brain

• Alzheimer's disease is characterized by anatomical changes, including the

development of amyloid plaques and neurofibrillary tangles.

• Amyloid plaques are a sticky buildup which accumulates outside the nerve cells in the

brain. Amyloid is a protein which is normally found throughout the body. In

Alzheimer ‘s disease, this protein begins to divide improperly creating a substance

called beta amyloid which is toxic to brain cells. As the beta amyloid builds up,

neuritic plaques develop and the brain cells begin to die.

• Neurofibrillary tangles are the second anatomical hallmark of AD. Normally, every

brain cell contains long fibers made of protein which act as scaffolds, holding the

brain cell in its proper shape and also helping transport of nutrients within the cell. In

AD, these fibers begin to twist and tangle. The brain cell loses its shape and also

becomes unable to transport nutrients properly; it eventually dies.

- These neurofibrillary tangles are resistant to chemical or enzymatic breakdown.They persist in brain tissue long after the neuron from which it arose has died

and disappeared!

Stages of Alzheimer Disease

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Stages of Alzheimer Disease

• Initial change is subtle

– Short-term memory loss – Mild changes in personality

– Randomly forget important and unimportantdetails

– Stage 1

• Last for 2 – 4 years

– Stage 2

• Very mild

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• Mild to moderate cognitive decline

– Stages 3 and 4• Performance issues in social or work

• Decline in the ability to plan and organize

• Seem subdued and withdrawn

– Stage 5 – moderately severe

• Assistance required for day to day activities

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– Stages 6 and 7

• Terminal stage

• Have to be institutionalized

•the last stage of the disease.

– Loss of ability to respond to the environment – Require total care

– Bedridden

• Death can occur as a result ofcomplications related to chronic debilitation.

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• Weight loss is a major concern for elderly

people with Alzheimer disease.

• Why?

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Huntington‘s disease

• Autosomal dominant inherited disorder

• Progressive degeneration of the cerebral

cortex and basal ganglia

• Decreased neurotransmitter – GABA and

GABA receptors

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• Symptoms begin at around the age of 40

• progressive dysfunction of intellectual and

thought process

• loss of working memory

• slow thinking

• restlessness and irritability• Chorea – progressive rigidity

• depression

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• Alzheimer and Huntington are diseases

under the group ‗dementia‖ – a

progressive degeneration of cognitive

function due to organic causes.

• What are the similarities and differences

between this 2?

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Parkinson Disease

• Etiology: – May be idiopathic, acquired or drugs

(chlorpromazine, thioridazine)

• Pathogenesis: – Dopamine deficiency in the basal

ganglia (substantia nigra) associated

with motor impairment;

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• Difficulty initiating and controlling

movements results in akinesia, tremor,

and rigidity

– Tremor occurs at rest and hand tremorsexhibit pill-rolling movements

– General lack of movement, loss of facial

expression, drooling, propulsive (shuffling)

gait, and absent arm swing

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Clinical Manifestations

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Genetic/immune related

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Genetic/immune related

diseases

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Demyelinating disorders

• Myelin sheath is destroyed but the axons

remain intact

• Remyelination does not occur to any

significant extent

• Caused by viral, chemical, or

immunological mechanisms

• Commonest demyelinating condition – is

MS

M lti l S l i (MS)

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Multiple Sclerosis (MS)

• A demyelinating disease of the CNS• Most common nontraumatic cause of

neurologic disability among young andmiddle-aged adults

• Characterized by exacerbations andremissions over many years in severaldifferent sites in the CNS

– Initially, there is normal or near-normalneurologic function between exacerbations.

– As the disease progresses, there is lessimprovement between exacerbations andincreasing neurologic dysfunction.

Incidence of MS

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Incidence of MS

• Affects 1-2 million people worldwide

• The onset of MS is usually between 20 and 40 years of age.

• Male/female ratio is about 1:2.

• MS is the most prevalent CNS demyelinating disorder and a leading cause

of neurological disability in early adulthood second only to trauma.

• The disease is most prevalent in areas far from the equator.

• MS occurs in all races but is more common in whites.

• Although the disorder does not exhibit a defined inheritance pattern, 15% of

all persons with MS have an affected relative.

- Disease susceptibility is linked to the HLA locus on chromosome 6 (HLA-DR2)

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Pathogenesis

• Interaction between the immune systemand the CNS

• previous virus infection in a genetically

susceptible individual

• Involves 2 stages:

– First stage – inflammation

– Extension, consolidation, demyelination and

gliosis

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Myelin Sheath Damage

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• An immune response causes initial and recurring inflammatory reactions.

• Plaques characteristically involve the CNS white matter but occasionally

extend into the adjacent gray matter. They often develop into larger

plaques.

First Stage:

• The acute (early) stage of plaque formation is characterized byinflammatory lesions. These lesions are small and widespread. Symptoms

usually remit, partially or completely, weeks after the onset of an earlyepisode

Second Stage:

• The chronic stage of demyelination and plaque formation is

characterized by gliosis (glial scarring with late degeneration of axons).• Progressive loss of function leads to permanent disability, usually over 20

years or so.

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Cli i l M if t ti

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• First symptoms – between 20 and 40years of age

• 4 categories of disease

– Relapsing – remitting (most common 85%)

– Secondary progressive disease

– Primary progressive disease

– Progressive relapsing (rare)• Clear exacerbations with or without recovery

phase


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• Depend on the location of damage:

– Motor dysfunction

– Sensory dysfunction

– Cranial nerve dysfunction

• Blurred vision, diplopia, dysphagia

– Sexual dysfunction

– Cerebellum dysfunction

L t i th di

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Late in the disease

• Classic triad described by Charcot in 1868 – Nystagmus

– Intention tremor

– Speech disorders• Spastic paraplegia, incontinence,

dementia, and extreme emotional labilityare also typical of the late stage

Diagnosis

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• There is no single test that confirms the diagnosis of multiple sclerosis, and there are a number of

other diseases with similar symptoms.

- The distribution of symptoms is important: multiple sclerosis affects multiple areas of the

body over time.

• The pattern of symptoms is also critical, especially evidence of the relapsing- remitting pattern, so

a detailed medical history is one of the most important parts of the diagnostic process .

• Most diagnostic criteria for MS require a history of exacerbations and remissions plus objective

demonstration by examination or testing of ≥ 2 separate neurologic abnormalities.

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ALS

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(Amyotrophic Lateral Sclerosis)• Classic ALS - Lou Gehrig disease• Degenerative disorder involving lower and upper motor motors neurons

resulting in progressive muscle weakness leading to respiratory failure and

death usually 2-5 years from symptom onset.

• ―Amyotrophic‖ refers to progressive muscle wasting

• The neurons that are affected in ALS are the motor neurons -- the nervesthat are responsible for controlling all voluntary movement. The motorneurons in the brain and in the spinal cord begin to degenerate, then to die,and are unable to send any messages to the muscles that they control. Themuscles begin to atrophy (shrink) and weaken and the person eventuallyloses the ability to use these muscles.

Cause remains unknown; genetic mutations possibleTypically occurs between 40 to 60 years and affects men more than women

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• Review the similarities and differences

between MS and ALS (Amyotrophic

Lateral Sclerosis)

Documents

CNS-unit 2