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Clinical Conditions II > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

Extrapyramidal Disorders

A 
affect the regulation of movement:
– initiation of movement
– speed of movement
– control or quality of the movement
– tremor
– whether movement is voluntary or not
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2
Q

Abnormal Movements

A

Tremor, Chorea, Athetosis, Dystonia, Balismus, Myoclonus and Tics

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3
Q

Types of Tremors

A
  • Physiological: normal (6-12)
  • Intention: during activity, cerebellar injury
  • Resting: associated with PD (4-6)
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4
Q

Chorea

A

– Involuntary rapid, irregular muscle jerks
– Associated with lesions of the caudate or putamen
– When strong, facial and tongue movements are also observed
– Voluntary movements can be distorted.

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5
Q

Unilateral Chorea

A

Hemiballismus

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6
Q

Dystonia & Athetosis

A

– Slow, purposeless, writhing movements (athetosis)
– Dystonia refers to those movements which are more like or turn into postures
– Not present during sleep; affected by stress and intention
– Associated with perinatal anoxia, CP, Huntington’s & drug side effect (inherited or acquired)

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7
Q

Myoclonus

A
  • Sudden, violent muscle jerks

- Can be spontaneous or brought on by sensory stimulation, arousal, or as part of a voluntary movement

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8
Q

Physiologic Myoclonus

A

nocturnal myoclonus & hiccups

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9
Q

Essential Myoclonus

A

isolated abnormality

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10
Q

Epileptic Myoclonus

A

manifestation of epilepsy

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11
Q

Symptomatic Myoclonus

A

Associated many neuro-degenerative and metabolic disorders (from cerebral cortex – brainstem –spinal cord)

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12
Q

Tics

A

– Sudden, recurrent, coordinated abnormal movements or verbalizations
• Occurs repeatedly and can be suppressed voluntarily for short periods
• Worsen with stress
• Diminished during voluntary movements or mental concentration, and disappear during sleep

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13
Q

Transient simple tics

A

common in children; usually go away within a year

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14
Q

Chronic simple tics

A

begin in childhood; benign but don’t go away

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15
Q

Tourette’s Syndrome

A

Chronic multiple motor and vocal tics

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16
Q

Involuntary Verbal Tics in Tourettes Syndrome

A

– Typical to include grunts, barks, hisses, or coughing.
– Coprolalia: vulgar or obscene utterances
– Echolalia: parroting of another’s speech
– Parilalia: repeating the same word over and over

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17
Q

Involuntary Motor Tics in Tourette’s Syndrome

A

– Blinking, grimacing, sniffing
• hopping, jumping, obscene gestures may develop
– Echopraxia: imitation of another’s movements
– Self mutilation (40-50%): biting nails, picking nose, pulling hair

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18
Q

Lesions of Basal Ganglia

A

• Decomposes behavior into isolated motor acts
• Decomposes intended motor acts into movements of inappropriate amplitudes
– Too little or too much amplitude

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19
Q

Idiopathic Parkinsonism

A

– Progressive, neurodegenerative disease

• Deficits due to loss of dopamine 2° degeneration of dopaminergic neurons in substantia nigra pars compacta

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20
Q

Two Major “Forms” of Parkinsonism

A

Tremor dominant and Akinetic

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21
Q

PIGD (Akinetic) Type Parkinsonism

A

more postural instability, gait difficulty -associated with a worse prognosis

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22
Q

Later Onset is more likely to cause

A

PIGD type

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23
Q

Risk Factors of Parkinson Disease

A

• Genetic, behavioral, and environmental factors are being examined

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24
Q

Genetic Risk Factors for Parkinson’s

A

– 5-10% with familial pattern of inheritance
– Role of alpha-synuclein protein due to change in
the gene SNCA (Lewy bodies)

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25
Q

Environmental Risk Factors for Parkinson’s

A

– Chemical toxins
Higher Risk: Rural Living
Lower Risk: Cigarette smoking, alcohol use, caffeine, physical activity, regular ibuprofen use, calcium channel blockers

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26
Q

Pathology of Parkinsonism

A

Widespread distribution of Lewy Bodies in the lower brainstem

27
Q

Long Prodromal Phase: Early non-motor signs (NMS) prior to Dx

A

– Olfaction involvement (hyposmia)
– Constipation
– REM sleep behavior disorder

28
Q

Cardinal Features of Sporadic PD

A
  • Tremor – resting “pill rolling”
  • Rigidity – cogwheel or lead pipe
  • Bradykinesia – slow movement
  • Postural instability
29
Q

Supportive Criteria of Parkinson’s

A
  • Unilateral onset with persistent asymmetry
  • Progressive
  • Response to dopamine therapy
  • Olfactory dysfunction
30
Q

Exclusion Criteria of Parkinson’s

A
  • Lack of benefit from dopamine
  • Current or recent use of dopaminergic blockers
  • Documentation of alternative cause: (Hydrocephalus, encephalitis, trauma, toxins, vascular disorder)
  • Physical exam
31
Q

Physical Exam findings that exclude a pt from Parkinson’s dx

A

– Cerebellar signs (ataxia, dysmetria)
– Early dementia
– Supranuclear gaze palsy
– PD limited to the LE’s for more than 3 yrs.
• Likely Lower Body Parkinsonism
– Less responsive to L-dopa and higher incidence of HTN
– Cortical signs (aphasia, apraxia, astereo-agnosia)

32
Q

Diseases that may look like Parkinson Disease

A
  • Progressive supranuclear palsy: progressive and fatal
  • Multiple system atrophy: progressive and fatal
  • Lewy body disease
33
Q

Progressive supranuclear palsy

A

– Idiopathic, degenerative, primarily affecting subcortical grey matter (dentate nucleus, pons, midbrain, BG)
– Failure of voluntary vertical gaze
– Postural instability
– Neck often assumes an extended posture
– Psuedopulbar palsy – facial weakness, dysarthria, dysphagia, increased jaw and gag reflexes
– Dementia - forgetfulness, slowed thought, changes in mood and personality

34
Q

How is Progressive supranuclear palsy distinguished from PD?

A

early falls, problems of downward gaze, extended neck posture, tremor uncommon in PSP and PD drugs are less effective in PSP

35
Q

Multiple system atrophy

A

– Wide-spread neuro degeneration
– MSA-P – neuronal loss in striatum and GP
• Bradykinesia; rigidity
– MSA-C – cerebellar degeneration
– Shy-Dragersyndrome: autonomic involvement
• Postural hypotension, anhidrosis, disturbance of sphincter control and impotence

36
Q

How is Multiple system atrophy distinguished from PD?

A

symmetric presentation and multi-system involvement

37
Q

Lewy body disease

A

– Form of dementia
– Cognitive changes lead to dementia and usually precede or occur shortly after the appearance of PD-like deficits
– Cognitive function may fluctuate markedly within a 24 hour period
– Postural hypotension and syncope

38
Q

How is Lewy Body disease distinguished from PD?

A

early cognitive involvement, symmetric deficits, and less likely to see tremor

39
Q

PD Voluntary Movement

A

• Akinesia
– No movement or
– Delay in initiation

• Bradykinesia
– Slow movement

• Hypokinesia
– Low amplitude movement

40
Q

Involuntary Movement PD

A

• Tremor
– Pill Rolling
– Resting
4-6 times/sec

• Rigidity
– Different than spasticity

41
Q

PD Walking

A
  • Flexed posture
  • Anterior displaced CM
  • Short, shuffling steps
  • Loss of associated movement
  • Festinating gait
42
Q

Standing Balance; Static - PD

A

Postural predisposition to loss of balance

43
Q

Dynamic Standing Balance- PD

A

– Impairments in preparatory postural adjustments

– Loss of righting and protective responses

44
Q

Mental Status in PD

A
  • Decline in cognitive function (usually significant declines occur later in the disease process)
  • Visual disturbances (hallucinations)
  • Depression
45
Q

Precursor of Dopamine

A

L-dopa

3-5 year max benefit

46
Q

What is the goal of taking medication with PD?

A

restoring balance between Ach & Dopamine

47
Q

What can brain stimulation help with?

A
  • dyskinesias

- may reduce rigidity

48
Q

Huntington’s Disease (chorea)

A
  • A progressive degenerative (of striatum) disorder
  • A hereditary disorder which manifests itself in early to mid adult life
  • Each child of an affected parent has a 50% chance of inheriting the gene that causes HD
  • Progressive and fatal: average lifespan is 15 years after clinical onset
49
Q

Clinical Findings of HD

A
  • Chorea: starts as restlessness, can’t suppress blinks, but progresses to choreiform movements
  • Motor impersistence (drop objects, cant hold tongue out, minor car accidents)
  • Dystonia
  • Dementia and emotional disturbances
  • With OCD and chorea, weight loss is a significant problem in HD
50
Q

Atypical or Westphal variant form and subtypes of HD

A

– Can show rigidity, akinesia (like PD)

– Juvenile form (before age 20) is rare but can show rigidity, akinesia along with other neurobehavioral symptoms

51
Q

Dementia and emotional disturbances in HD

A

– Earliest changes consist of irritability, moodiness, and antisocial behavior
– Later – OCD, impairment of attention and executive function with
eventual psychosis, consistent with frontostriatal pathology
– Depression (potentially many years)
– Personality issues

52
Q

Hemiballismus

A
  • Sudden (acute) onset of flinging – choreic movements (implicating proximal muscle involvement)
  • Typically thought to be due to a lesion of the subthalamic nucleus in the basal ganglia (usually as a result of a CVA)
53
Q

Tardive Dyskinesia

A
  • Choreo-athetoid movements of the face, mouth, jaw and tongue
  • Grimacing, pursing the mouth, writhing movements of the tongue, and “fish-gaping”
  • Associated with prolonged use of psychotropic drugs
54
Q

Role of Cerebellum in Movement

A
  • Balance and Eye Movements
  • Skilled Voluntary Movement
  • Locomotion
  • Muscle Tone (hypotonia is common with damage)
55
Q

Typical signs and symptoms of damage to the cerebellum

A
  • Incoordination
  • Delays in movement initiation and termination
  • Hypotonia
  • Intention tremor
  • Dysequilibrium and vertigo
56
Q

Ataxia (Incoordination)

A

• Loss of ability to control and coordinate movements

57
Q

Ataxia is often associated with

A

– Delays in initiation
– Dysmetria: errors in the range of movement (Hypometria or hypermetria)
– Dysdiadochokinesia (Errors in rate and regularity of movement)

58
Q

Etiologies of Damage to Cerebellum

A
  • Toxins
  • Genetic Diseases (Friedreich’s Ataxia)
  • System Degeneration (Olivopontocerebellar atrophy)
  • Structural Diseases (Tumors)
  • Demyelinating Disease (MS)
59
Q

Friedreich’s Ataxia

A
  • One of the most common hereditary disorders of the nervous system
  • Disrupts normal assembly of amino acids into proteins
  • Progressive degeneration of – Dorsal root ganglia, large myelinated axons of peripheral sensory nerves, Corticospinal tracts, Dentate nuclei
60
Q

Friedreich’s Ataxia average age of onset

A

13 years

61
Q

Friedreich’s Ataxia Sxs

A
  • Ataxia begins in lower limbs (gait ataxia) but progresses up
  • Nystagmus and dysarthria
  • Impairment of sensation; later LE weakness (UMN and LMN)
  • Scoliosis
62
Q

Olivopontocerebellar Atrophy

A

Combined degeneration of the cerebellum, pons, and

inferior olives

63
Q

Olivopontocerebellar Atrophy Sxs

A

• Progressive ataxia with a later onset than Friedreich’s ataxia
• Gait is usually affected first with resultant decreased movement speed and balance deficits
• Dysarthria, muscle spasms, weakness and autonomic
disorders are also common: Urinary incontinence; orthostatic
hypotension

64
Q

B1 (thiamine) deficiency

A

Wernicke-Korsakoff

oculomotor abnormalities; mental status; ataxia of stance and gait

Clinical Conditions II (11 decks)

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