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Neurosurgery > Neurologic examination > Flashcards

Neurologic examination Flashcards

1
Q

What are the six parts of the neurologic examination?

A

1) Sensorium and behaviour.
2) Posture and gait.
3) Postural reactions.
4) Spinal reflexes, muscle mass, and muscle tone.
5) Cranial nerves.
6) Cutaneous sensation.

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2
Q

What areas of the neurologic system are responsible for normal sensation?

A

Cerebrum and reticular activating system (nuclei collected throughout the brainstem)

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3
Q

What are the 4 altered levels of mentation?

A

1) Depression - slight decreased arousal
2) Obtundation - decreased arousal but responds to voice or touch
3) Stupor - arousal only to vigorous stimuli, response is incomplete or inadequate
4) Coma - unresponsive to stimuli

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4
Q

Altered sensation or mentation suggest what neurolocalization?

A

Intracranial

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5
Q

What disorders could cause recumbency?

A

Brainstem, cervical spinal cord, diffuse neuromuscular disease (only brainstem should affect sensorium)

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6
Q

What are the two postures that severe intracranial lesions may cause?

A

Decerebrate rigidity: opisthotonus and rigid extension of all limbs. Severe impact on mentation. Secondary to midbrain or rostral cerebellar lesions.

Decerebellate rigidity: opisthotonus and rigid extension of limbs with flexion of hip joints. May not impact mentation. Secondary to lesions of the cerebellum.

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7
Q

What components of posture should be assessed as part of the neurologic examination?

A

Head tilt (vestibular disease)
Head or body turn (forebrain disease)
Neck position (cervical spinal cord or neuromuscular disease)
Hock angle
Trembling (neuromuscular)
Tail position (flaccid with LS disease)

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8
Q

How can gait abnormalities by broadly classified?

A

Ataxia: disturbances in the vestibular, cerebellar or proprioceptive systems

Weakness: UMN or LMN

Lameness: LMN or orthopedic

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9
Q

Do forebrain lesions typically result in gait abnormalities?

A

No

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10
Q

Describe the modified Frankel score

A
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11
Q

Lesions in what location cause a gait disturbance?

A

Lesions at the level of the midbrain or caudal to it

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12
Q

Is UMN or LMN paresis typically associated with generalized proprioceptive ataxia?

A

UMN paresis, as the descending UMN pathways are closely associated with the ascending proprioceptive pathways

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13
Q

What are the three forms of ataxia?

A
  1. Generalized proprioceptive: UMN lesions of the spinal cord or mid to caudal brainstem.
  2. Cerebellar: hypermetria +/- head tilt, loss of balance, nystagmus
  3. Vestibular: falling to one side, incoordination
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14
Q

Do lesions caudal to the brainstem result in ipsilateral or contralateral paresis and proprioceptive ataxia?

A

Ipsilateral

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15
Q

How can peripheral and central vestibular ataxia be distinguished?

A

Peripheral: No proprioceptive ataxia. May have Horner’s and facial nerve deficits due to close association of CNVII and sympathetic tracts to the middle ear.

Central: Ipsilateral proprioceptive ataxia and paresis. May have CNVII and CNV deficits (cranial nerve nuclei are close to the vestibular nuclei).

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16
Q

What is the pathway responsible for postural reactions?

A

Starts with sensory nerves of the peripheral nervous system, enters the spinal cord via the dorsal roots, proprioceptive information ascends in the ipsilateral dorsal and dorsolateral funiculi of the spinal cord. Information remains ipsilateral to the level of the midbrain where conscious proprioceptive information is then relayed to the contralateral thalamus and cerebral hemisphere.

Also relies on UMN and LMN tracts to be intact for appropriate response.

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17
Q

What are some tests that can be performed to assess postural reactions?

A

Hopping, extensor postural thrust, hemiwalking, wheelbarrowing, paw replacement.

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18
Q

Localize the lesion based on the following flow-chart.

A
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19
Q

Localize the lesion based on the following flow-chart.

A
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20
Q

What are the components of a normal reflex arc?

A

Intact afferent (sensory) arm comprised of the sensory receptor, sensory nerve, dorsal nerve root, and spinal cord segment.
Intact efferent (motor) arm comprised of the lower motor neuron unit.

The afferent and efferent arms enter and exit the spinal cord within the same spinal cord segments.

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21
Q

What spinal cord segments does the patellar reflex test?

A

Spinal cord segments L4-L6 (femoral nerve)

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22
Q

How can the patellar reflex response be graded?

A

Absent (0), hyporeflexive (+1), normal (+2), hyperreflexive (+3) or clonic (+4)

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23
Q

What spinal cord segments does the biceps tendon reflex test?

A

C6-C8 (musculocutaneous nerve)

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24
Q

What spinal cord segments does the triceps tendon reflex test?

A

C7-T2 (radial nerve)

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25
Q

What spinal cord segments does the withdrawal reflex test?

A

Thoracic limbs: C6-T2 (radial, musculocutaneous, median, ulnar, dorsal thoracic axillary)

Pelvic limbs: L6-S1 (sciatic nerve)

26
Q

What gait is common with a lesion involving solely the sciatic nerve?

A

Plantigrade stance, exaggerated flexion of the hip (can appear hypermetric)

27
Q

What does a crossed extensor reflex indicate?

A

UMN lesion on the side ipsilateral to the leg extension

28
Q

What nerves innervate the perineal reflex?

A

The sacral nerve and caudal segments of the spinal cord through the pudendal nerve.

29
Q

What is the pathway for the cutaneous trunci reflex?

A

Regional segmental spinal nerves carry sensory impulses into the spinal cord where they are relayed cranially to C8-T1, a synapse occurs with the lower motor neurons of both lateral thoracic nerves which innervate the cutaneous trunci muscle.

Reflex is elicited from the thorax caudally to the level of the wings of the ilium. Preserved for 1-2 vertebral bodies caudal to the level of the spinal cord lesion.

30
Q

Why does muscle hypertonia result from UMN disease?

A

Descending UMN influence provides inhibition of extensor musculature. When this is disrupted LMN are released from inhibition

31
Q

Is LMN or UMN disease more likely to result in neurogenic atrophy?

A

LMN disease.

32
Q

Describe the function of the various cranial nerves

A
33
Q

At what age does the menace response first become present?

A

10-12 weeks.

34
Q

What nerves does the menace response test?

A

The optic nerve and the facial nerve (ability to close the eyelid). Most of the visual pathway is contralateral to the eye being tested.

35
Q

What does an absent direct ocular PLR but present indirect PLR indicate?

A

An optic nerve or retinal defect in the eye with the absent direct PLR.

36
Q

What does an absent direct and indirect ocular PLR indicate?

A

Lesion affecting the parasympathetic oculomotor nerve nucleus of CNIII or iris muscular disorder (menace response should be present).

37
Q

If vision is intact but menace is negative what nerve could be affected?

A

The facial nerve as this innervates the orbicularis oculi muscle that is responsible for closure of the eyelid

38
Q

What are the clinical signs of Horner’s?

A

Enophthalmus, miosis, ptosis and prolapse of the third eyelid

39
Q

Describe the pathway for Horner’s syndrome

A

Preganglionic neurons are distributed in the thoracolumbar spinal cord (T1-T3), they leave the spinal cord and join the vagus to form the vagosympathetic trunk coursing in the carotid sheath. They synapse in the cranial cervical ganglia ventromedial to the tympanic bulla before heading to innervate the dilator muscles of the pupil of the iris. An UMN system also facilitates function of the preganglionic sympathetics, beginning in the hypothalamus and descending in the lateral funiculus of the spinal cord. Disruption at any level can cause Horner’s.

40
Q

Why does otitis media commonly result in Horner’s and facial nerve paralysis?

A

Close anatomic relationship between the sympathetic fibers and axons of the facial nerve in the tympanic bulla

41
Q

What is positional ventral strabismus commonly associated with?

A

Vestibular disease

42
Q

What is resting or spontaneous nystagmus most commonly associated with?

A

Vestibular disease

43
Q

What does the palpebral reflex test?

A

The sensory branches of the trigeminal nerve (afferent arm) and the motor branches of the facial nerve (efferent arm)

44
Q

A drooping of the lip or ear indicates dysfunction of which nerve?

A

The facial.

45
Q

What does a dropped jaw indicate?

A

Bilateral mandibular nerve dysfunction (trigeminal nerve branch)

46
Q

What does nasal hypalgesia indicate?

A

Ipsilateral trigeminal nerve lesion or contralateral prosencephalic lesion

47
Q

What does an absent gag reflex indicate?

A

Dysfunction of the glossopharyngeal or vagus nerves. Dysphagia may also be evident.

48
Q

Describe the cutaneous sensory areas of the thoracic limb.

A

Median nerve: palmar surface of the paw

Ulnar nerve: palmer surface of the paw, lateral surface of digit 5, caudal surface of the antebrachium.

Musculucutaneous nerve: medial surface of the brachium.

Radial nerve: dorsal surface of the paw and cranial and lateral antebrachium.

49
Q

Describe the cutaneous sensory areas of the pelvic limb.

A

Fibular and tibial nerves (terminal branches of sciatic): dorsal and plantar surfaces of the paw

Saphenous nerve (branch of femoral): medial aspect of the pelvic limb and digit 1.

50
Q

In a patient with an isolated sciatic nerve injury what might be expected with stimulation of the medial paw?

A

Flexion of the hip joint due to innervation of the ilipsoas muscle with spinal cord segments L1-L4 and the rectus femoris with the femoral nerve. Stifle, tarsus and digits will not flex

51
Q

What are the 4 functional regions of the spinal cord?

A

Cranial cervical (C1-C5)
Cervicothoracic (C6-T2)
Thoracolumbar (T3-L3)
Lumbosacral (L4-S3/caudal)

52
Q

With a spinal cord lesion in what order is function lost?

A

Loss of proprioception, voluntary motor function, voluntary bladder function, and nociception.

53
Q

What lesion localization does a “two engine gait” suggest?

A

C6-T2

54
Q

What is the Schiff-Sherrington phenomenon?

A

Peracute T3-L3 spinal cord lesion that produces markedly increased extensor tone in the thoracic limbs. This is due to loss of ascending inhibitory axons arising from interneurons at L1-L4.

55
Q

How do you differentiate between Schiff-Sherrington and C1-C5 lesion?

A

Postural reactions will be normal with Schiff-Sherrington

56
Q

What is spinal shock?

A

T3-L3 spinal cord lesions associated with LMN signs. Often accompanied by Schiff-Scherrington.

Typically transient (hours to days).

57
Q

Where are motor neurons location?

A

In the ventral grey matter of the CNS

58
Q

What are the components of the lower motor neuron unit?

A

Neuron in the ventral gray matter of the CNS, ventral nerve root, spinal nerve, nerve plexus, named nerves of the limb, NMJ, and muscle.

59
Q

What diseases can cause LMN disease?

A
  1. Junctionopathies (myasthenia gravis)
  2. Neuropathies (acute polyradiculoneuropathy).
  3. Myopathies (hypokalemic myopathy).
60
Q

Do patients with LMN disease typically have ataxia?

A

No, because the general proprioceptive pathways are unaffected.

61
Q

In a study by Nagendran 2024 in JVIM, was head turn associated with an ipsilateral or contralateral forebrain lesion? Was this consistent for lesions of the cerebullum, or cervical spinal cord?

A

Yes - head turn was ipsilateral to forebrain lesions.

Cerebellar lesions had contralateral head tilts but ipsilateral head turns and body turns, and cervical spine lesions were associated with contralateral head tilt, body tilt, and head turn.

Neurosurgery (11 decks)

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