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Neurology > MS & Parkinsons > Flashcards

MS & Parkinsons Flashcards

1
Q

MS is characterized by

A

autoimmune disease characterized by:
•inflammation
•demyelination
• gliosis
* (leads to sclerotic plaques-hardened patch like areas found on autopsy throughout the CNS.
* Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes)
*Glia, also called glial cells or neuroglia, are non-neuronal cells in the central nervous system (brain and spinal cord) and the peripheral nervous system that do not produce electrical impulses. They maintain homeostasis, form myelin, and provide support and protection for neurons.

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2
Q

Cardinal s/s: Charcot’s Triad

A

•Intention tremor
• Scanning speech (normal speech rhythm broken up)
•Nystagmus
( Charcot also added paralysis)

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3
Q

MS onset demographics

A
  • typically btw 20-40 year olds
  • rare in children and people under 50
  • white> black, Asian, Native American
  • increased risk with an affected family member
  • not an inherited disease but has a genetic susceptibility
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4
Q

Virus and auto immune response

A

•when people with genetic susceptibility are exposed to a viral agent the immune system responds with activated myelin-reactive lymphocytes

Implicated viruses under investigation:
•Epstein-Barr
•Measles 
• Canine distemper
•Herpes
•Chlamydia pneumonia
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5
Q

MS immune response

A

when the immune response of a genetically susceptible person is triggered:
trigger -> cytotoxic (myelin-reactive lymphocytes) affects to the CNS myelin -> demyelination and acute inflammation
*surviving oligodendrocytes (type of neuroglia that support and insulate axons) may produce remyelination
* demyelinated areas undergo gliosis -> glial scars (plaques) axon undergoes neurodegeneration
* lesions of white matter (myelinated) always occurs, however, lesions of gray matter may be present in more advanced disease

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6
Q

Areas of pathological prediliction

A
  • optic nerves
  • periventricular white matter
  • cerebellar penduncles
  • Spinal cord
  • Corticospinal tract
  • posterior/ dorsal columns
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7
Q

clinical course

A

highly variable clinical course depending on site:
•early limb weakness, blurring of vision (optic nerve), uncoordinated, abnormal sensations
• exacerbations and long asymptomatic remissions

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8
Q

Diagnosis of MS

A
  • evidence of damage must be present in at least 2 separate areas of the CNS
  • damage must have occurred at 2 separate points in time at least 1 month apart
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9
Q

System of criteria for dx

A

McDonald criteria

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10
Q

Dx tests

A
  • MRI- detects plaques in the CNS- new areas of active inflammation present as “bright spots”. Long term lesions may be seen as “black holes”. 95% of pts with clinically defined MS have well defined MRI changes, 5% do not. Other diseases can exhibit similar lesions and healthy individuals can have bright spots.
  • 90% of individuals have decreased conduction (leads to fatigue) in the presence of dymelination * visual, auditory, and somatosensory pathways
  • MS pts have increased CSF immunoglobulin levels
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11
Q

Types of MS progression: Highly variable

A

1) benign MS *fewer than 20% of cases: stable periods with little relapse exacerbation periods that then calm and return the level of the disease to its former level i.e. no progression
2) Relapsing-remitting MS *most common, approx 85% of patients: stable periods that turn into exacerbation relapse periods before returning to a stable period but at a more progressed stable level than prior to the exacerbation i.e. slow but steady progression
3) Secondary chronic progression *typically preceded by relapsing-remitting course: a stable time followed by a spike followed by a progressed stable period and eventually altering to be just a steady phase of progression i.e. slow but steady progression before phasing into a constant steadily progressing phase
4) Primary progressive *rare approx 10%: no stable periods just a constant steady progression

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12
Q

relapsing remitting MS (RRMS)

A

symptom flare ups followed by recovery; stable btw attacks

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13
Q

Secondary progressive (SPMS)

A

2nd phase of relapsing-remitting: progressive worsening of symptoms with or without superimposed relapses- treatment may delay this phase

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14
Q

Primary progressive MS (PPMS)

A

gradual but steady accumulation of neuro problems from onset

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15
Q

Benign MS

A

few attacks and little to no disability after 20 years

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16
Q

Progressive relapsing (PRMS)

A

approx 5% of cases

progressive course from onset combined with occasional acute symptom flare ups

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17
Q

Malignant/exacerbating factors for MS

A

Relapses/exacerbations- new and recurrent MS symptoms lasting >24 hours
Factors that lead to exacerbation periods:
•viral or bacterial infections- cold, flu, UTI, sinus infection
•Diseases of organ systems- hepatitis, pancreatitis, asthma
•stress

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18
Q

Uthoff’s/Pseudoexacerbation

A

temporary worsening of MS symptoms: s/s FATIGUE
• episodes typically come and go within 24 hours
•increased body temp can trigger pseudo attacks
•effects are usually immediate and dramatic

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19
Q

MS meds: Acute relapses

A

Acute relapse meds:

•Corticosteroids (methylorednisolone)- used to treat acute disease relapses (exacerbations), decrease the duration of the episode. Exert powerful anti-inflammatory and immunosupressive effects.

AE- HTN, hyperglycemia, osteopenia, DM, skin thinning, aseptic femoral necrosis

•Plasmaphoresis (plasma exchange)- used to enhance recovery from an acute response in patients who don’t respond to steroids

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20
Q

MS meds: disease modifying therapeutic agents

A

• Synthetic Interferon (betaseron, extavia, avonex, rebif)- used to slow down immune response by decreasing inflammation, swelling, and rapid proliferation of T + B cells. Blocks activated T cells from crossing the blood brain barrier and damaging myelin. Decreasing relapses and number of lesions, decreases attack severity, but can’t reverse existing defecits.

AE: flu-like symptoms, depression, allergic and liver reactions.

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21
Q

MS meds: for spasticity

A

MS spasticity meds:

•Baclofen- helps to decrease spasticity

AE: drowsiness, weakness, fatigue,

•Botulinum toxin- localized muscle relief for increased tone and spasticity

AE: excessive use can overly weaken muscles

•diazepam- valium

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22
Q

MS surgical treatments

A

Surgery: for intractable spasticity
•Tendonotomy: severing tendon
•Neurectomy: severing nerves
•Rhizotomy: severing nerve roots

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23
Q

MS meds: for pain

A
  • Meds for pain: trycyclic antidepressants
  • For paroxysmal pain: Carbamazepine (Tegretol), amitryptyline (Elavil), phenytoin (Dilantin), diazepam (Valium), gabapentin (Neurontin)
  • For dyesthesias (painful itchy burning): amitryptyline (Elavil)
  • Trigeminal neuralgia: Carbamazepine (Tegretol)
  • Spasticity and spasm pain: acetominophen (Tylenol), ibprofen (Advil)
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24
Q

MS sensory impairments

A

Altered rather than complete loss of any single sensation is more common
•Paresthesias- numbness, tingling, pins and needles
•Vibration sense LE impairments are also common
• Visual impairments (common in approx 80% of patients)
•Optic neuritis- inflammation of the optic nerve producing an ice pick pain behind the eye with blurring or graying of vision or blindness in one eye
• Scotoma- dark spots that may occur in the center of the visual field
• Nystagmus- due to cerebellar vestibular involvement
•Diplopia- double vision due to discoordination of ocular muscles
• 20% of patients will develop pressure injuries

25
Q

MS pain

A
  • 80% of MS patients will experience pain
  • often pain is acute, paroxysmal of sudden, spontaneous onset, which is often intense, sharp, shooting, electrical, shock-like and burning

Most common types of pain are:
•Trigeminal neuralgia (Tic Doulaureux)- demyelination
of sensory division of CN V, triggers face pain

•Lhermitte’s sign

•Paroxysmal limb pain- Dyesthesias- abnormal burning, aching sensation, worse at night, after exercise, aggravated by increased temp
tx: hydrotherapy, pressure stockings, or gloves (relieved by pressure- H2O temp between 80-85° F)

  • Hyperpathia- light, sensory stimuli causes severe pain
  • HA- migraine or tension type
  • Chronic Neuropathic pain- results from demyelinating lesions in spinothalamic tracts
  • Musculoskeletal pain- muscle and ligament strain
26
Q

Lhermitte’s sign

A

common sign of posterior column damage in the spinal cord. Flexion of the neck produces an electric shock-like sensation running down the spine and into the LEs
Tx: cervical collar to limit neck flexion

27
Q

Fatigue MS

A

fatigue is an extreme issue for MS patients
• worsens throughout the day
• comes on abruptly
• aggravating factors: physical exertion, heat and humidity, disturbed or decreased sleep, depression, infections
• side effects of medications: analgesics, anticonvulsants, antidepressants, anti HTN, anti-inflammatory
Tx: ed in energy conservation, avoid overwork, activity pacing, meds for fatigue-amantadine (symmetral, modofinil (provigil)

28
Q

Pseudobulbar affect

A

sudden uncontrollable bouts of laughter or crying without reason
*occurs sometimes in MS patients

29
Q

MS spasticity

A

occurs in 75% of MS patients especially in LEs. Fluctuates daily, exacerbated by fatigue, stress, increased temp, infections, and noxious stimuli

30
Q

Parkinson’s

A

chronic, progressive disorder of the nervous system characterized by the cardinal s/s; rigidity, bradykinesia, tremor, postural instability.

31
Q

Parkinson’s cardinal s/s

A
  • rigidity
  • bradykinesia
  • tremor
  • postural instability
32
Q

Parkinson’s demographic

A

average age of onset is 50-60 y/o
young onset= 21 to 40 y/o
M>F
Onset is insidious with slow progression

33
Q

Parkinson’s causes and etiology

A

Primary disturbances in the dopamine systems of the basal ganglia.

Parkinson’s disease is caused by a loss of nerve cells in the part of the brain called the substantia nigra of the basal ganglia

Nerve cells in this part of the brain are responsible for producing a chemical called dopamine.

Dopamine acts as a messenger between the parts of the brain and nervous system that help control and co-ordinate body movements.

If these nerve cells die or become damaged, the amount of dopamine in the brain is reduced.

This means the part of the brain controlling movement cannot work as well as normal, causing movements to become slow and abnormal.

The loss of nerve cells is a slow process. The symptoms of Parkinson’s disease usually only start to develop when around 80% of the nerve cells in the substantia nigra have been lost.

Thought to be caused by a mix of genetic and environmental causes though this is unsure. It is rare for a parent to pass Parkinson’s on to their child. Exposures to pesticides and herbicides may increase risk.

34
Q

Non-motor Parkinson symptoms:

A

Non-motor Parkinson symptoms may precede motor symptoms by years:
• Anosmia (loss of smell)
•Constipation
• Rapid eye movement (REM), sleep behavior disorders, (daytime somolence, insomnia, dream enacting)
•OH
• Mood disorders
• excessive saliva (sialorrhea)
•integumentary changes (seborrhea- oily skin, diaphoresis, decreased ability to dissipate heat)
•difficulty speaking (microphonia-weak voice, and mutism) and dysphagia
•cognitive problems- bradyphrenia- slow thought, confusion, and sometimes dementia

35
Q

Parkinson’s subgroups

A

2 distinct Parkinson’s subgroups

1) tremor predominant- typically have fewer problems with bradykinesia or postural instability
2) postural instability and gait- disturbed predominant

36
Q

Speech and swallowing MS deficits

A
  • Speech problems due to: weakness, spasticity, tremor, ataxia. Affects 40% of MS patients
  • Dysarthria: slurred
  • Ataxic: Scanning speech
  • Dysphonia: change in voice quality- hoarseness, breathiness, hypernasal
  • Swallowing deficits : Dysphagia- due to poor coordination of tongue and oral muscles
  • Signs of swallowing dysfunction: difficulty chewing and maintaining lip seal, inability to swallow, spitting or coughing during or after meals
  • Aspiration pneumonia is a serious complication, signs include: wet quality with gurgling or sounds of congestion and fever. Most common cause of death
37
Q

MS cognitive issues

A

50% of MS patients have cognitive symptoms such as: •impairments in short-term memory, attention, concentration, information processing, executive functions, visuospatial functions and verbal fluency.
•Long –term memory, conversational skills, and reading comprehension are typically intact.
•50% of patients with MS with MS experience a major depressive episode.
•Affective disorders present in 10% of MS patients and include changes in mood, feelings, emotional expression, and control.
•Pseudobulbar effect- sudden and unpredictable episodes of crying, laughing or other emotional displays.
•Euphoria- exaggerated feeling of well- being

38
Q

MS bowel and bladder impairments

A

urinary bladder dysfunction occurs in 80% of MS patients.
Types of bladder dysfunction include:

  • Small, spastic bladder- failure to store
  • Flaccid or big bladder- failure to empty
  • Dyssynergic bladder- problem between bladder contraction and sphincter relaxation
  • Emptying dysfunction with large residual volumes -> UTI

Constipation is the most common bowel complaint

39
Q

Basal ganglia function

A

Involved in…
Initiation and regulation of gross intentional movements
•Planning and execution of complex motor responses
•Facilitation and inhibition of selective movement responses
•Ability to perform automatic movements and postural adjustments
•Maintaining normal background muscle tone by inhibition of motor cortex and brainstem.

40
Q

Parkinsonism etiology

A

encompasses several disorders with primary disturbances of the dopamine systems of the basal ganglia
Disorders:
• Parkinson’s disease/Idiopathic parkinsonism- the most common form of parkinsonism
•Secondary parkinsonism- due to a number of identifiable causes:
- post encephalitic Parkinsonism: slow virus from influenza epidemics
- toxic Parkinsonism: pesticides, manganese, carbon monoxide, cyanide, MPTP (synthetic heroin)
- drug induced Parkinsonism: neuroleptic (thorazine, haldol); antidepressants, antihypertensives, withdawal usually reverses symptoms

41
Q

Parkinson-Plus Syndrome

A

Group of neurodegenerative diseases affecting the substantia nigra and produce Parkinsonian suymptoms

  • Shy-Drager, Progressive Supranuclear Palsy, Multi-infarct vascular disease, Diffuse Lewy body disease, Normal Pressure Hydrocephalus.
  • Diseases present with rigidity and bradykinesia, but other diagnostic symptoms usually appear- i.e dementia. They typically do not show improvement with L-dopa
42
Q

Hoehn & Yahr Classification of Disability

A

I. Minimal or absent; unilateral if present
II. Minimal bilateral or mid-line involvement. Balance not impaired
III. Impaired righting reflexes. Unsteadiness when turning or rising from chair. Some activities are restricted, but patient can live independently and continue some form of employment
IV. All symptoms present of severe. Standing and walking only possible with assistance.
V. Confined to bed or wheelchair

43
Q

Parkinson’s meds

A

• Levadopa/Cabidopa (Sinmet): controls bradykinesia and rigidity.
AE: dyskinesia, dystonia, hypotension, dizziness, arrhythmias, hallucinations, insomnia, dysuria (pain and/or difficulty with urination), depression

•Dopamine Agonist: reduces rigidity and bradykinesia
AE: dizziness, hallucinations, constipation, increased risk of impulse disorders

•Anticholinergics: treats moderate tremor and dystonia (involuntary muscle contractions that cause repetitive movement)
AE: dizziness, blurred vision, dry mouth, urinary retention

•Monoamine Oxidase B Inhibitors: may slow, but not stop, disease progression, has lower risk of dyskinesias
AE: dizziness, OH, hallucinations, insomnia

44
Q

Parkinson’s nutrition

A
  • increased calorie, and decreased protein (protein blocks effectiveness of L-dopa)
  • no more than 15% of calories from protein
  • protein in evening meals when activity decreases
  • increased daily intake of H2O and dietary fiber to decrease constipation
45
Q

Rigidity

A
  • Cogwheel rigidity: jerky, ratchet-like resistance

* Leadpipe rigidity: sustained resistance with no fluctuations

46
Q

Rigidity progression of Parkinson’s

A

Rigidity begins asymmetrically (early stages)
• typically affects proximal muscles of the shoulder and neck first and progresses to muscles of the face and extremities
• decreased ability to move easily and decreased arm swing and rotation leading to increased energy expenditure
•increased by active movement, mental concentration, and emotional stress

47
Q

Parkinson’s disease autonomic dysfunction and neuropsychiatric disturbances

A

autonomic dysfunction:
• OH
•Constipation and bladder dysfunction
• sexual dysfunction

neuropsychiatric disturbances:
•depression
• dementia
•psychosis

48
Q

Rigidity treatment

A
  • rocking
  • slow, rhythmic rotation
  • side-lying rolling
  • RI
  • diaphragmatic breathing with exercise
  • cognitive imaging, medications, relaxation
  • dim lighting
  • neutral warmth
  • reciprocal movements
49
Q

Bradykinesia and hypokinesia

A

Bradykinesia- slowness of movement
Hypokinesia- decreased amplitude of movement
• insufficient recruitment of muscle force during initiation of movement
•Results in prolonged movement and reaction times
•Bradyphrenia- slowness of thought may contribute

50
Q

Freezing episodes

A

in gait triggered by confrontation of competing stimuli (narrowed space, obstacles…) can be overcome with additional strategies or behavioral tricks using external cues e.g. MARCH, WALK BIG

51
Q

Bradykinesia and hypokinesia treatment

A
  • LSVT BIG- repetitive high amplitude movements working at high intensity 8/10 BORG, 1 hour / 4x per week for 4 weeks, with homework
  • visual cues
  • rhythmic auditory stimulation
  • auditory cues- big steps, march
  • self assessment
  • videotape so they can see their amplitude
  • external perturbations are generally contraindicated
52
Q

Postural instability and gait disturbances

A

•Abnormality of postures and balance- usually not seen in early stages – especially in those patients who are tremor dominant
•Abnormal postural responses- postural setting, equilibrium, turning, stopping, starting responses
increased with narrowing of BOS and competing attention/ dual tasks
•Visuospatial and medication side effects contribute
•Clinical measures: BERG, Functional Reach. TUG, Cognitive TUG, DGI
•PD and elderly tend to use hip rather than ankle strategies to destabilization forces

53
Q

Postural instability balance treatment

A
  • try to duplicate conditions in everyday life
  • dynamic stability tasks: weight shifts, reaching, rotation of the head and trunk, rotation with reaching
  • focus on faster initiation and execution movement times
  • external perturbations are generally contraindicated as they tend to increase postural stiffness
  • “kitchen sink” exercises: heel rises, toe offs, partial wall squats, and chair rises, single limb stance, back kicks, marching in place, wii balance
54
Q

Postural instability and gait

A

Approximately 13- 33% of patients present with postural instability and gait disturbance as their initial motor symptom. Also present in the late stage of tremor dominant patients
Presents with reduction in arm swing
Abnormal stooped posture contributes to festinating gait with progressive increase in speed with shortening stride which requires taking multiple short steps to catch up with COM to prevent falling.
Anteropulsive- forward festinating gait
Retropulsive- backward festinating gait
Freezing episodes

55
Q

Postural instability and gait treatment

A

Improve slow speed and decreased stride length
•“Walk tall” “Walk fast” “Swing arms”
•Large step and arm swing commands are more effective instructional strategies
•Brisk marching music
•Treadmill with harness, pole walking, walking on different surfaces/ terrains, curbs, stairs, ramps-especially while carrying out other task –i. e. garbage bins to curb
•Practice strategies for freezing

56
Q

Postural changes- decreased flexibility

A
  • weakness of anti-gravity muscles, stooped posture, COG anterior
  • increased hip, knee, neck, and trunk flexion- changes COM placing it forward over limit of stability
  • Contractures: hip and knee flexion, hip adductors, PF, shoulder adductors and IR, elbow flexors
57
Q

Parkinson’s and osteoporosis

A

reduced activity levels and poor nutrition= osteoporosis, which combined with decreased equilibrium reactions results in falls and fractures. Within 10 years of dx of Parkinson’s approx. 25% of patients will have had a hip fracture.

58
Q

Postural changes- decreased flexibility treatment

A

•stretching= caution with osteoporosis and edematous tissue (LEs)
•bilateral symmetrical D2FUE with coordinated breathing (for respiratory compromise restricted disease due to rigidity)
• positioning is important be careful with prone positioning and respiratory compromise
• stretch tight muscles, strengthen weak
p. 791

59
Q

Other Parkinson’s

A

Sensory (6th: 813, 822; 7th; 767,789)
Dysphagia (6th:813; 7th:767-768)
Speech (6th:814, 842; 7th: 768,800)
Cognitive (6th: 814; 7th: 768)
Depression and Anxiety (6th:814, 843; 7th: 768797, 802)
*Autonomic dysfunction (6th: 814-815, 826-827; 7th: 769, 786) Orthostatic Hypotension- 7th: 786
Sleep disorders (6th:815, 7th: 769
Dyskinesias (6th:826; 7th: 785-786 )
Function /ADL (6th: 827,836-837; 7th: 786-787792-794)
Adaptive/ Supportive devices (6th: 843; 7th: 801-802)

Neurology (9 decks)

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