Module E-06 Flashcards

1
Q

Hallmark features of disordered movement include:

A

1) Impaired postural reflexes that would normally contribute to balance (either during movement or while stationary).
2) Diminished or slowed movements (hypokinesia/bradykinesia).
3) Excessive involuntary movements (hyperkinesia).
4) Uncoordinated or unsteady movements (ataxia).

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2
Q

4 types of involuntary movements

A

1) Tremor
2) Chorea
3) Athetosis
4) Ballismus

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3
Q

What are tremors?

A
  • Alternating contraction of opposing muscles
  • Forms of tremor are varied and hence have differing causes. Some tremors are effectively benign, whereas others reflect significant pathology
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4
Q

What is chorea?

A
  • involves brief, purposeless, irregular jerky movements of body parts
  • Voluntary behaviors (e.g., walking) may be affected, as choreatic movements become disruptive. The expression of successive choreatic movements resembles dancing – hence the term “chorea”
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5
Q

Most common reason for Chorea

A

often stemming from basal gangliar disease

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6
Q

Describe Athetosis

A

comprises continuous slow writhing of body parts

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7
Q

Most common reason for Athetosis

A

often related to basal gangliar pathology

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8
Q

Describe Ballismus

A

“Flinging” and rotatory movements involving the limbs are characteristic.

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9
Q

Most common reason for Ballismus

A

Causal lesions often affect the subthalamus, which contributes to basal gangliar function

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10
Q

What differentiates Hypokinesia in Lower vs Upper motor lesions

A
  • Lower motor neurons or the neuromuscular junction can be implicated, with hypokenesis presenting as flaccid
    paralysis.
  • Lesions of upper motor neurons, which often yield elevated muscular tone and hence hyperreflexia.
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11
Q

What causes hypokinesia in Parkinson’s?

A
  • Dysfunction involves modulatory/regulatory circuits
  • The basal ganglia are not regulated normally by the mesencephalic substantia nigra.
  • correlates with impaired initiation of movement, rigidity, poor postural reflexes and slowing of movement (i.e., bradykinesia).
  • Perhaps paradoxically, patients expressing Parkinson disease and hence hypokinesia/bradykinesia often exhibit resting tremor
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12
Q

What type of interactions between Sensory and motor systems cooperate to maintain equilibrium?

A

o Some sensory-motor interactions are largely reactive.

o Other such interactions involve predictive or anticipatory circuitry.

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13
Q

Decorticate posture

A
  • a cerebral lesion affecting the corticospinal and corticobulbar systems with sparing of motor centers of the brainstem.
  • In such cases, the disinhibited red nucleus of the midbrain increases tone of the flexor muscles of the upper limbs, while pontine and medullary motor centers (in the absence of cerebral influence) independently promote extension
    of the legs.
  • The posture, if not tonically expressed, may be elicited by noxious stimuli.
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14
Q

Decerebrate posture

A
  • the muscle tone of the arms favors extension (resulting from the loss of red nuclear output).
  • Remaining disinhibited brainstem motor centers continue promoting extension of the legs.
  • The posture, if not tonically expressed, may be elicited by noxious stimuli.
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15
Q

What is Station?

A

The ability of the patient to stand steadily with the feet together

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16
Q

How is Gait assessed?

A
  • The patient attempts to walk in a straight path (usually in the absence of special visual cues such as lines on the floor).
    -The task may be repeated while the patient walks in tandem (heel-to-toe) or preferentially on either the heels or the toes.
  • The ability of the patient to turn smoothly while
    reversing direction should be assessed.
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17
Q

Categories of tremors

A

1) Resting tremor- typically becomes more apparent when the patient is otherwise motionless (i.e., at rest).
2) Intention (kinetic) tremor becomes apparent with purposeful movement (e.g., reaching for a glass).

3) Essential tremor (benign familial tremor) commonly prompts misdiagnoses of cerebellar or Parkinson disease, as it can resemble intention or resting tremor.
4) Postural tremor may arise only when a particular posture is assumed (e.g., when the arms are outstretched with the palms up.

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18
Q

In what syndrome is a resting tremor seen?

A
  • Parkinson disease, although not all patients will exhibit the phenomenon
  • The resting tremor may diminish at later stages of the disease.
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19
Q

What causes intention(kinetic ) tremor?

A

Cerebellar lesions

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20
Q

Describe intention tremor

A
  • Tremor becomes apparent with purposeful movement (e.g., reaching for a glass).
  • The amplitude of the intention tremor tends to increase as the affected body part approaches the target in space.
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21
Q

Hallmark motoric manifestations of Parkinson’s disease

A
  • resting tremor
  • bradykinesia
  • Facial Masking
  • Rigidity
  • Loss of Postural Reflexes
  • Parkinsonian Gait
  • Loss of Habituation to Glabellar Stimulation
  • Speech
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22
Q

What are the Prodromal manifestations of Parkinson’s?

A

o Hyposmia
o Autonomic dysfunction - Erectile, Cardiac and GI
o Rapid eye movement sleep disorder- Maintenance or breakthrough of muscular rigor during dream
sleep

23
Q

What does Hyposomia indicate?

A

Indicates degeneration of olfactory bulbs

24
Q

What does the Rapid eye movement sleep disorder indicate?

A

Reflects pontine degeneration

25
Q

What is Akinesia?

A

reflects the absence of movement (or limited movement – as in hypokinesia)

26
Q

What is Bradykinesia

A

refers to movements that are

pathologically slower than normal. In Parkinson disease, initiation of movement may be particularly difficult

27
Q

What is Facial Masking?

A

Facial expression commonly diminishes, resulting in a masked appearance

28
Q

Describe the Rigidity in Parkinsonism

A
muscular rigidity (stiffness) of differing forms, as revealed during assessment of passive movement.
o Cogwheel rigidity refers to the recurrent stepwise release and return of resistance to passive movement.
o Lead-pipe rigidity refers to resistance that is sustained
throughout a range of passive movement.
29
Q

Describe the Loss of Postural Reflexes in Parkinsonism

A

disruptions of station do not provoke corrective postural adjustment, and patients fall.

30
Q

Describe the Parkinsonian Gait in Parkinsonism

A
  • Patients taking short shuffling steps.
  • Turning is difficult, and many small steps replace smooth pivoting.
  • Unintentional acceleration may arise (festination).
  • A slight push from the back may yield propulsive steps, whereas a push from the front may trigger retropulsion.
  • Gait may normalize with sensory cues (parallel lines on floors or rhythmic acoustic stimuli)
31
Q

Describe the Speech in Parkinsonism

A

speech tends to be quiet, hoarse, and monotonous but

occasionally with accelerative bursts (festination of speech)

32
Q

What is the glabellar reflex?

A

The glabellar reflex involves noxious stimulation (firm tapping) between the eyes to elicit bilateral blinking. The ophthalmic branch of cranial nerve V serves as the sensory limb of the reflex, whereas the temporal branches of cranial nerve VII constitute the motor limb.
In neurologically intact persons, blinks weaken with repeated stimulation.

33
Q

Describe the Loss of Habituation to Glabellar Stimulation in Parkinsonism

A

In neurologically intact persons, blinks weaken with repeated stimulation. Such habituation does not readily occur in Parkinson disease.

34
Q

Traditional Stages of Parkinson Disease (with the exclusion of prodromal manifestations)

A
  1. Unilateral
  2. Bilateral but with preserved postural reflexes
  3. Bilateral with loss of postural reflexes (falls becoming more likely)
  4. Severe disability but with some movement
  5. Akinesia
35
Q

Differential Diagnosis for resting tremor of Parkinson Disease

A
o Essential (postural) tremor differs in that it may only be expressed when a particular posture is maintained
o Intention tremor often indicates cerebellar disease rather than Parkinson disease
36
Q

Conditions that mimic Parkinson’s disease

A
o Iatrogenic
o Postencephalitic
o Stroke-induced
o Drug-induced
o Neoplast
37
Q

5 types of HYPERkinetic disorders

A

1) Chorea
2) Athetosis
3) Dystonia
4) Ballismus
5) Tic Syndromes

38
Q

2 Diseases that manifest in Choretic movements

A

1) Huntington disease - autosomal dominant condition.
2) Sydenham disease - a transient disorder that bears autoimmune characteristics with a link to childhood rheumatic fever.

39
Q

Condition where Athetoid movements are seen

A

athetoid cerebral palsy

40
Q

Athetosis accompanies __________

A

hemiplegia, with a hemiplegic gait therefore

being superimposed

41
Q

What is Hemiballismus?

A

the condition is unilateral with manifestations expressed contralateral to the injury

42
Q

What are Dystonias?

A

Involve muscle spasms or sustained abnormal postures

43
Q

What are Generalized Dystonias?

A

Abnormal postures involving the trunk and limbs.

44
Q

What are Spasmodic torticollis?

A

a specific dystonia involving the neck. In this

condition, neck muscles (e.g., sternocleidomastoid) contract involuntarily and may become hypertrophic

45
Q

Most dystonias are ________ or _________

A

Partial;segmental

46
Q

What are Tics?

A

irregularly occurring stereotyped movements that are usually transient and coordinated. They range from simple (e.g. eye blinking, arm jerks) to more complex (head shaking, spitting, floor-licking).

47
Q

What is Tourette’s Syndrome

A

A genetic disorder with an onset about seven years of age, is a specific form of tic disorder.

48
Q

Symptoms of Tourette’s Syndrome?

A

o Multifocal tics are common and often accompany attention deficit hyperactivity disorder.
o Key to the diagnosis of Tourette syndrome is a vocal tic (e.g., barking, grunting).

49
Q

3 Drug induced Movement disorders

A

1) Tardive dyskinesia
2) Dopa-induced dyskinesia
3) Drug-induced Parkinsonism

50
Q

What drug causes Tardive Dyskinesia?

A

some antipsychotic drugs (dopamine receptor antagonists)

51
Q

Manifestations of Tardive Dyskinesia

A
  • The condition commonly features stereotypic oral movements.
  • Advanced age of patients predicts greater vulnerability.
  • Dyskinesia does not necessarily abate with drug withdrawal, perhaps becoming permanent.
52
Q

What drug causes Dopa Induced Dyskinesia?

A

often arises during treatment of Parkinson disease with the precursor to dopamine.

53
Q

Manifestations of Dopa Induced Dyskenesia

A

Choreatic movements predominate, but facial dystonias (e.g., grimacing or eye closure) are not uncommon.

54
Q

What drugs cause Drug induced Parkinsonism?

A

Can arise with agents that suppress dopaminergic transmission. The symptoms dissipate within weeks of
withdrawal of these agents.