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632 Advanced Anesthesia Health Assessment > Neuro Handouts > Flashcards

Neuro Handouts Flashcards

1
Q

Location of lesion that causes Spasticity

A

Upper motor neuron or the corticospinal tract

  • Increased muscle tone (hypertonia) is rate dependent.
  • Tone increases when passive movement is rapid, & decreases when passive movement is slow.
  • Tone is also greater at the extremes of the movement arc.
  • During rapid passive movement, initial hypertonia may give way suddenly as the limb relaxes
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2
Q

Common causes

of spasticity of upper motor neuron or the corticospinal tract

A
  • Stroke, especially late or chronic stage
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3
Q

Location of lesion that causes Rigidity

A

Basal Ganglia System

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4
Q

Describe Rigidity

A
  • Increased resistance that persists throughout the movement arc, independent of rate of movement, is called lead-pipe rigidity.
  • During flexion & extension of the wrist or forearm, a superimposed ratchet-like jerkiness is called Cogwheel rigidity & can be due to underlying tremor
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5
Q

Common causes of Rigidity

A
  • Parkinsonism
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6
Q

Location of lesion that causes Flaccidity (or Hypotonia)

A
  • Lower motor neuron system at any point from the anterior horn cell to the peripheral nerves, & in cerebellar disease
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7
Q

Describe Flaccidity (or Hypotonia)

A
  • Loss of muscle tone (hypotonia) causes the limb to be loose or floppy.
  • The affected limbs may be hyperextensible or even flail-like
  • Flaccid muscles are often weak
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8
Q

Common causes of Flaccidity (or Hypotonia)

A
  • Guillain-Barre syndrome; initial phase of spinal cord injury (spinal shock)
  • Stoke
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9
Q

Location of lesion that causes Paratonia

A
  • Both hemispheres in the frontal lobes
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10
Q

Describe Paratonia

A
  • Sudden, irregular changes in tone accompany passive range of motion
  • Sudden loss of tone that increases the ease of motion is called FACILITATORY paratonia
  • Sudden increase in tone making motion more difficult is called OPPOSITIONAL paratonia
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11
Q

Common causes of Paratonia

A
  • Dementia
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12
Q

What are the 3 components of the GCS

A
  • Eye opening
  • Motor Response
  • Verbal Response
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13
Q

GCS: Eye opening

A

4 - Spontaneous: eyes open, not necessarily aware
3 - To speech: nonspecific response, not necessarily to command
2 - To pain: pain from sternum/limb/supraorbital pressure
1 - None: even to supraorbital pressure

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14
Q

GCS: Motor response

A

6 - Obeys commands: follows simple commands
5 - Localizes pain: arm attempts to remove supraorbital/chest pressure
4 - Withdrawal: arm withdraws to pain, shoulder abducts
3 - Flexor response: withdrawal response or assumption of hemiplegic posture
2 - Extension: shoulder adducted & shoulder & forearm internally rotated
1 - None: to any pain; limbs remain flaccid

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15
Q

GCS: Verbal response

A

5 - Oriented: Converses & is oriented
4 - Confused: converses but confused, disoriented
3 - Inappropriate: intelligible, no sustained sentences
2 - Incomprehensible: moans/groans, no speech
1 - None: no verbalization of any type

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16
Q

Small or Pinpoint Pupils

A
  • Bilaterally small (1-2.5 mm) suggest damage to the sympathetic pathways in the hypothalamus, or metabolic encephalopathy, a diffuse failure or cerebral function that has many causes, including drugs
17
Q

Pinpoint pupils < 1 mm

A
  • Suggest a hemorrhage in the pons, or the effects of morphine, heroin, or other narcotics
18
Q

Midposition Fixed Pupils

A
  • Pupils that are in the midposition or slightly dilated (4-6 mm) & are fixed to light
  • Suggest structural damage in the midbrain
19
Q

Bilaterally Large fixed & dilated pupils

A
  • Severe anoxia & its sympathomimetic effects, as seen after cardiac arrest
  • May also result from ATROPINE - like agents, phenothiazines, or tricyclic antidepressants
20
Q

Bilaterally Large reactive pupils

A
  • May be due to cocaine, amphetamine, LSD, or other sympathetic nervous system agonists
21
Q

One large fixed & dilated pupil

A
  • Warns of herniation of the temporal lobe, causing compression of the oculomotor nerve (CN III) & midbrain
  • May also be seen in diabetic patients from infarction of CN III
22
Q

Cerebral Cortex lesion Motor signs & symptoms

A
  • Chronic contralateral corticospinal - type weakness & spasticity
23
Q

Cerebral Cortex lesion Sensory signs & symptoms

A
  • Contralateral sensory loss in the face, limbs, and trunk on the same side as the motor deficits
24
Q

What can cause cerebral cortex motor & sensory deficits

A
  • Cortical stroke
25
Q

Brainstem lesion motor signs & signs

A
  • Chronic contralateral corticospinal weakness & spasticity plus CN deficits such as diplopia (from weakness of the extraocular muscles) & dysarthria
26
Q

Brainstem lesion Sensory signs & signs

A
  • Variable depending on the level of brainstem
27
Q

What can cause Brainstem motor and sensory deficits

A
  • Brainstem stroke

- MS plaque

28
Q

Spinal cord lesion motor signs & symptoms

A
  • Weakness & spasticity, but often affecting both sides (when cord damage is bilateral), causing paraparesis or quadriparesis depending on the level of injury
29
Q

Spinal cord lesion sensory signs & symptoms

A
  • Dermatomal sensory deficit on the trunk on one or both sides at the level of the lesion, and sensory loss from tract damage below the level of the lesion
30
Q

What can cause Spinal cord motor and sensory deficits

A
  • Trauma

- Spinal cord tumor

31
Q

Subcortical Gray Matter: Basal Ganglia lesion motor signs & symptoms

A
  • Slowness of movement (bradykinesia), rigidity, & tumor
32
Q

Subcortical Gray Matter: Basal Ganglia lesion sensory signs & symptoms

A
  • Sensation not affected
33
Q

What can cause Subcortical Gray Matter: Basal Ganglia motor and sensory deficits

A
  • Parkinsonism
34
Q

Cerebellar lesion motor signs & symptoms

A
  • Hypotonia, ataxia, nystagmus, dysdiadochokinesis, & dysmetria
35
Q

Cerebellar lesion sensory signs & symptoms

A
  • Sensation not affected
36
Q

What can cause Cerebellar motor and sensory deficits

A
  • Cerebellar stroke

- Brain tumor

632 Advanced Anesthesia Health Assessment (12 decks)

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