Neurology- Tone Flashcards

1
Q

Tone examination

A
  • ask the patient to lie supine in the bed and relax.
  • enquire about pain
  • passively move each joint through as full ROM as possible, both slowly and quickly in all anatomically possible directions
  • be unpredictable with these movements, in both direction and speed to prevent the patient actively moving with you. We want to assess passive tone
  • it may be helpful to distract the patient by asking them to count backwards whilst assessing tone.
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2
Q

Time examination- upper limb

A
  • hold the patients hand as if shaking, use your other to support their elbow
  • assess tone at the wrist/elbow with supination/pronation and flexion/extension moments
  • activation is a technique used to exaggerate subtle increase in tone and is particularly useful for assessing extrapyramidal side effects
    • ask patient to describe circles in the air with the contralateral limb while assessing tone. An increase in tone is normal
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3
Q

Tone examination- lower limb

A
  • roll the leg from side to side then briskly flip the knee to into fixed position, observing movement in the foot
  • Typically, the heel moves up the bed, but increased time may cause it to lift off the bed for to failure of relaxation
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4
Q

Tone examination- ankle clonus

A
  • support the patients leg, with both the knee and the ankle resting in 90’
  • briskly dorsiflex and partially evert the foot, sustaining the pressure. Clonus is felt as repeated beats of dorsiflexion/plantar flexion
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5
Q

Tone examination- Myotonia

A
  • ask the patient to make a fist and then relax and open their hand. Watch for speed of relaxation
  • using a tendon hammer, percuss the belly of the thenar eminence
  • this may induce contraction of the muscles, causing the thumb to adduct, and you may witness dimpling of the muscle belly
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6
Q

Hypotonia

A
  • decreased tone may occur in lower motor neuron lesion and is usually associated with muscle wasting, weakness and hyporeflexia
  • it may also be a feature of cerebellar disease or signal the early phase of cerebral or spinal shock when the paralysed limbs are atonic prior to developing spasticity
  • reduced tone can be difficult to elicit
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7
Q

Hypertonia- spasticity and rigidity

A
  • increased time may occur in 2 main forms: spasticity and rigidity
    -spasticity- velocity dependent resistance to passive movement, it is detected with wick movements and is a feature if upper motor lesions
  • it is usually accompanied weakness, hyperflexia, extensor plantar response
  • it is more evident on extension in the upper limbs and flexion in the legs
  • rigidity is a sustained resistance throughout the ROM and is easily detected when the limb is moved e.g. PD
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8
Q

Power- examination

A
  • don’t have to test every muscle
  • ask about pain and observe from then in the chair
  • ask the patient to lift arms above head
  • ask them to play piano- asymmetrical finger may be early sign of cortical or extrapyramidal disease
  • observe the patient with arms out (palms out) and eyes closed, check for protinator drift when one arm starts to protonate
  • ask if they can overcome gravity, then apply pressure on a single limb
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9
Q

Power

A
  • upper motor neuron lesions produce weakness of a large group of muscles
  • lower motor neuron damage causes paresis of an individual muscle so detailed examination is required
  • Look for patterns that suggest a diagnosis
  • in pyramidal weakness (e.g. post stroke) extensors are weaker in upper limb than flexors and vice verse in lower limbs
  • myopathies tend to cause proximal weakness and neuropathies cause distal patterns
  • radiculopathies tend to cause focal weakness
  • very few organic disease causes power to fluctuate (fatiguable) e.g. myasthenia
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10
Q

Deep tendon reflexes- anatomy

A
  • a tendon reflex is the involuntary contraction of a muscle in response to stretch
  • it’s mediated mediated by a reflex of afferent (sensory) and efferent (motor) neurons
  • muscle stretch activates the muscle spindles that lead to direct efferent impulses causing contraction
  • ## most important reflexes are deep tendon and plantar response
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11
Q

Tendon reflex exam

A
  • ask the patient to lie supine
  • strike your finger that is palpating the bicep and supinator tendon or the tendon itself for the tricep, knee and ankle jerk
  • record: as increased, decreased, normal, present with reinforcement or absent
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12
Q

Principal (deep tendon) reflexes

A
  • ensure that both limbs are positioned identically with the same amount of stretch. This is especially important for ankle is passively doriflexed before striking
  • compare each reflex. Check for symmetry
  • ## reinforce where it appears absent
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13
Q

Hoffmanns reflex

A
  • place your right index finger under the distal interphalangeal joint of the patients middle finger
  • use your thumb to flick the patients finger downwards
  • look for reflex flexion in the patients thumb
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14
Q

Plantar response

A
  • run a blunt object along the lateral border of the sole of the foot upto the little toe
  • normal is the great toe should move down.
  • extensor plantar response (babinski) signifies an abnormal reflex due to an upper motor neuron lesion
  • coincides with contraction of other leg flexor muscles
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15
Q

Tendon reflex’s meaning

A
  • hyperflexia is a sign of upper motor neuron damage
  • diminished or absent jerks are most commonly due to lower motor neuron lesions
  • in healthy older people ankle jerk may be lost and in myotonic pupils are associated with loss of some reflex’s
  • isolated loss of reflex suggests radiculopathy/mononeuropathy e.g. loss of ankle jerk= compression of S1 (disc prolapse)
  • an inverted biceps reflex= root pathology at the spinal level (C5)
  • Hoffmann reflex and increased finger jerks suggest hypertonia
  • in cerebellar disease the reflexes may be Pendigo and muscle contraction and relaxation tend to be slowed
  • ## plantar extension is a sign of upper motor neuron damage and is usually associated with other signs such as spasticity, clonus and hyper-reflexia
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