Neuromuscular and Neurological System Flashcards
Upper Motor Neuron Syndrome - Clinical Definition
What is upper motor neuron syndrome?
Upper motor neuron syndrome (aka, upper motor neuron disease) is a collection of signs and symptoms that result from injury to the upper motor neurons or anywhere along the descending motor control pathways (i.e., upper motor neuron pathways).
*Note: Examples of conditions that reflect upper motor neuron syndrome include traumatic brain injury, cerebrovascular accident (aka, stroke), spinal cord injury, multiple sclerosis, cerebral palsy, and Parkinson’s disease. Be aware that amyotrophic lateral sclerosis (ALS) reflects both upper and lower motor neuron syndromes.
Reference:
- Purves (6th ed.), pp.358,403
Upper Motor Neuron Syndrome - Etiology
In general, what causes upper motor neuron syndrome?
Injury to the cell bodies of the upper motor neurons at the:
- Cerebral cortex
- Motor control centers in the brainstem (aka, brainstem centers)
- Example: Reticular formation
Injury anywhere along the upper motor neuron pathways (aka, descending motor control pathways), which terminate in either the:
- Spinal cord
- The spinal cord terminates at the conus medullaris around the level of the L1 or L2 vertebra.
- The corticospinal tract and descending motor control pathways of the brainstem centers terminate in the spinal cord.
- Brainstem
- The corticobulbar tract terminates in the brainstem.
References:
- For information about motor control centers in the brainstem, see Purves (6th ed.), p.381, 397-398. In particular, see Purves (6th ed.), p.398 for information about the reticular formation.
- For more information about the decescending motor pathways (i.e., corticobulbar and corticospinal [aka, pyramidal] tracts), see Purves (6th ed.), p.384.
Upper Motor Neuron Syndrome - Clinical Presentation
What are the hallmark signs and symptoms of upper motor neuron syndrome?
Volitional movement:
-
Diffuse (i.e., generalized) paresis or paralysis of volitional movements of the “parts” (e.g., monoplegia, hemiplegia, paraplegia, quadriplegia [aka, tetraplegia]), NOT of individual muscles
- Paresis or paralysis will NOT be in a cranial nerve, myotomal, or peripheral nerve pattern.
Tone:
-
Hypertonicity or spasticity
- Exceptions are cases of spinal shock.
- Decrebrate or decorticate rigidity may be present
Sensory:
-
Diffuse (i.e., generalized) sensory loss
- Sensory loss will NOT be in a dermatomal or cutaneous nerve pattern.
- Loss of proproception and kinesthesia
Reflexes:
-
Increased or brisk deep tendon reflexes (DTR)
-
Clonus may be present
- May present with DTR assessment grades of 4/5 (“non-sustained clonus”) or 5/5 (“sustained clonus”)
-
Clonus may be present
- Babinski sign (*see image below) or Hoffman sign
Reference:
- WASHU “Neuroscreening” lecture from ECS I
- Purves (6th ed.), pp.403-405

Lower Motor Neuron Lesion - Clinical Presentation
What is lower motor neuron syndrome?
Lower motor neuron syndrome (aka, lower motor neuron disease) is a collection of signs and symptoms that result from injury to the lower motor neurons or their peripheral axons.
*Note: Examples of conditions that reflect lower motor neuron syndrome include Guillain-Barré syndrome, myasthenia gravis, and peripheral neuropathies (e.g., carpal tunnel syndrome). Be aware that amyotrophic lateral sclerosis (ALS) reflects both lower and upper motor neuron syndromes.
Reference:
- Purves (6th ed.), pp.376-377
Lower Motor Neuron Lesion - Clinical Presentation
In general, what causes lower motor neuron syndrome?
Injury to the cell bodies of the lower motor neurons at the:
- Brainstem motor nuclei (aka, cranial nerve nuclei)
- Ventral (anterior) horn of the spinal cord gray matter
Injury anywhere along the peripheral axons of lower motor neurons:
- Cranial nerves (e.g., spinal accessory nerve, or cranial nerve XI)
- Spinal nerves (e.g., C5 spinal nerve)
- Peripheral nerves (e.g., median nerve)
References:
- Purves (6th ed.), p.357
- For information about the relationship between spinal nerves and peripheral nerves, see Moore et al., (8th ed.), pp.52-53.
Lower Motor Neuron Lesion - Clinical Presentation
What are the hallmark signs and symptoms of lower motor neuron syndrome?
Volitional movement:
-
Focal paralysis of the individual muscles being supplied by cranial nerves, spinal nerves, and peripheral nerves
- Spinal nerve: Paralysis will be in a myotomal pattern.
- Cranial and peripheral nerves: Paralysis will only occur in muscles that are innervated by the affected nerve.
Tone:
- Hypertonicity, or flaccid paralysis
Sensory:
-
Focal sensory loss
- Spinal nerve: Sensory loss will be in a dermatomal pattern
- Cranial and peripheral nerves: Sensory loss will be in the cutaneous innervation pattern specific to the affected nerve. No dermatomal pattern of sensory loss.
- Intact proproception and kinesthesia
Reflexes:
-
Slow deep tendon reflexes (DTRs), or areflexia (i.e., absent reflexes)
- May present with DTR assessment grade of 0/5 (“no reflex”)
References:
- WASHU “Neuroscreening” lecture from ECS I
- Purves (6th ed.), pp.376-378, 403
Decerebrate and Decorticate Rigidity
What is decrebrate rigidity and decorticate rigidity?
Decerebrate and decorticate rigidity refer to hypertonic extension or flexion (respectively) in response to painful stimuli. These abnormal responses are due to damage to the upper motor neurons and the descending motor control pathways (i.e., upper motor neuron pathways).
-
Decerebrate rigidity (aka, decerebrate posturing) refers to excessive tone in the arm and leg extensor muscles. Decerebrate rigidity is commonly associated with damage to the upper brain stem (i.e., above the level of the medulla oblongata).
- Clinical presentation: (1) Arms and legs stiffly extended, (2) jaw clenched, and (3) neck retraction (*see image A).
-
Decorticate rigidity (aka, decorticate posturing) refers to excessive tone in the arm flexor muscles. Decorticate rigidity is commonly associated with damage to the cerebral cortex or the corticospinal tract.
- Clinical presentation: Arms flexed, adducted, and internally rotated; clenched fists (*see image B).
References:
- Purves (6th ed.), p.405, 495, G-8
- Louis et al. (13th ed.) (keywords: “decerebrate rigidity,” “decorticate rigidity”)
- See lecture on neurological lesions from Neuroscience.

Spinal Shock
What is spinal shock?
Spinal shock refers to the initial, short-lived period of flaccid paralysis, loss of deep tendon reflexes, and autonomic dysfunction (e.g., bowel and bladder reflexes, significant fall in arterial blood pressure) that is associated with damage to upper motor neurons or their descending motor control pathways as a result of an acute spinal cord injury. With spinal shock, all cord functions below the transection become substantially depressed.
- The phenomenon of spinal shock reflects the decreased activity of the spinal neural circuits (i.e., ensembles of neurons in the spinal cord) suddenly deprived of input from the cerebral (motor) cortex and brainstem. After several days, however, the spinal cord neural circuits regain much of their function for reasons that are not fully understood, and a pattern of signs and symptoms consistent with upper motor neuron syndrome emerges.
References:
- Purves (6th ed.), p.403, G-28
- Goodman and Fuller (4th ed.), p.1563 (“Changes in Muscle Tone”), 1564 (Box 34-1)
Oscillopsia
What is oscillopsia?
Oscillopsia refers to the inability to fixate on visual targets while the head is moving. Oscillopsia is the result of a loss of the vestibulo-ocular reflex (VOR) that is associated with vestibular damage.
Reference:
- Purves (6th ed.), p.316
What is the vestibulo-ocular reflex (VOR)?
The vestibulo-ocular reflex (VOR) refers to involuntary movement of the eyes that counter head movements during displacement of the head. This reflex allows the gaze to remain fixed on a particular point.
Reference:
- Purves (6th ed.), p.313, G-33
Naming of Spinal Nerves
How are spinal nerves named as they exit the vetebral spine?
Cervical segmental level
-
Eight cervical spinal nerves: C1-C8
- C1 spinal nerve exits above the C1 vertebra.
- C2-C7 spinal nerves exit between the vertebra superior to the spinal cord level and the vertebra at the same spinal cord level (e.g., C2 spinal nerve exits between C1-C2 vertebrae, C7 spinal nerve exits between C6-C7 vertebrae)
- C8 spinal nerve exits between C7-T1 vertebrae.
Thoracic and lumbar segmental levels
- Twelve thoracic spinal nerves: T1-T12
- Five lumbar spinal nerves: L1-L5
- The thoracic and lumbar spinal nerves exit between the vertebra at the same spinal cord level and the vertebra inferior to the spinal cord level (e.g., T1 spinal nerve exits between T1-T2 vertebrae, L5 spinal nerve exits between L5-S1 vertebrae).
Sacral and coccygeal segmental levels
- Five sacral spinal nerves: S1-S5
- One coccygeal nerve
- S1-S4 spinal nerves exit through the anterior and posterior sacral foramina between the vertebra at the same spinal cord level and the vertebra inferior to the spinal cord level (e.g., S1 spinal nerve exits through the sacral foramina between the S1-S2 vertebrae, S4 exits through the sacral foramina between the S4-S5 vertebrae).
- S5 spinal nerve and coccygeal nerve exit through the sacral hiatus.
References:
- Moore et al. (8th ed), pp. 129-130
- Netter Plate 161: Relation of Spinal Nerves to Spinal Vertebrae
- See Netter Plate 157 for a review of the bony anatomy of the sacrum and coccyx.

Cranial Nerves - Mnemonics
What are the three mnemonics to remember when thinking about the cranial nerves?
Number order of cranial nerves:
- “On old Olympus’s towering top, a Finn and German viewed some hops.”
Functional fiber types for each cranial nerve:
- “Some say marry money but my brother says big brains matter more.”
Origin or termination of each cranial nerve:
- CMPM
- 2244
CN I - Clinical Definition
What is cranial nerve I (i.e., CN I)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve I refers to the olfactory nerve.
The olfactory nerve directly enters the cerebrum.
The olfactory nerve contains special sensory fibers.
The olfactory nerve is responsible for the sense of smell (aka, olfaction).
References:
- Moore et al. (8th ed.), p.1069 (“Olfactory Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4)
CN I - Etiology
What can cause injury to cranial nerve I (i.e., CN I)?
Neurodegenerative diseases such as Parkinson’s disease (early onset) and Alzheimer’s disease
References:
- Medscape: Olfactory Dysfunction as a Diagnostic Marker for Parkinson’s Disease (https://www.medscape.com/viewarticle/714329_5)
- Louis et al. (13th ed.) (keyword: “anosmia”)
- Coach K’s Lecture Materials –> Neuromuscular III
CN I - Special Tests
What is a special test or cluster of tests to rule in or rule out injury to cranial nerve I (i.e., CN I)?
Test procedure:
- Instruct the patient to close off one nostril with a finger. Present to the open nostril a common, non-irritating odorant (e.g., coffee, soap, tobacco, orange), and ask if the patient smells something. Repeat with the other nostril.
Interpretation of results:
- Patient smells something = sense of smell is intact; no injury to CN I
- Patient doesn’t smell something = anosmia (i.e., a complete loss of odor detection); injury to CN I on the same side of the tested nostril
- Example: Patient cannot smell with the right nostril = right CN I involvement
References:
- Nolan, pp.45-46
- NeuroLogic Exam: Cranial Nerve > Anatomy (https://neurologicexam.med.utah.edu/adult/html/cranialnerve_anatomy.html#01)
- NeuroLogic Exam: Cranial Nerve Exam (https://neurologicexam.med.utah.edu/adult/html/cranialnerve_normal.html#01)
CN II - Clinical Definition
What is cranial nerve II (i.e., CN II)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve II refers to the optic nerve.
The optic nerve enters the cerebrum (i.e., cerebral cortex of the occipital lobe).
The optic nerve contains special sensory fibers.
The optic nerve is responsible for the sense of vision.
References:
- Moore et al. (8th ed.), pp.1070-1072 (“Optic Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4)
CN II - Etiology
What can cause injury to cranial nerve II (i.e., CN II)?
- Optic neuritis (i.e., inflammation of the optic nerve) secondary to multiple sclerosis
- Optic neuritis is often the first manifestation of multiple sclerosis.
- Occlusion of the middle cerebral artery (e.g., as during middle cerebral artery syndrome)
- Occlusion of the posterior cerebral artery (e.g., as during posterior cerebral artery syndrome)
References:
- Louis (13th ed.) (keyword: “Acute, Slowly Remitting Visual Loss”)
- Goodman and Fuller (4th ed.), p.1484 (“Multiple Sclerosis–Clinical Manifestations”), 1515 (“Posterior Cerebral Artery Syndrome”)
- O’Sullivan et al. (7th ed.), p.598 (“Middle Cerebral Artery Syndrome”), 599 (Table 15.3)
CN II - Special Tests
What is a special test or cluster of tests to rule in or rule out injury to cranial nerve II (i.e., CN II)?
TEST FOR VISUAL ACUITY
-
Test procedure:
- Test each eye using a Snellen chart.
-
Interpretation of results:
- Normal visual acuity = 20/20
- Abnormal visual acuity = recorded as appropriate based on Snellen chart (e.g., 20/70)
- Due to impairment of the eye structures (e.g., the lens as with cataracts, the macula [especially the fovea] as with macular degeneration, or CN II as with optic neuritis) on the same side as the tested eye
- Myopia, hyperopia, or presbyopia may be present.
TEST FOR VISUAL FIELDS
-
Test procedure:
- Test each eye with the confrontation test.
-
Interpretation of results:
- Accurate and consistent reporting of the number of fingers in each visual quadrant = normal visual field
- Inaccurate and inconsistent reporting of the number of fingers in one or more of the visual quadrants = visual field deficit
- Visual field deficits are determined based on where along the primary visual pathway the injury is. See “Visual Field Deficits” flashcard.
TEST FOR LIGHT REFLEX
-
Test procedure:
- Test each eye with the general light reflex test, or both eyes with the swinging flashlight test.
-
Interpretation of results:
- Normal light reflex = constriction of pupils in both eyes when testing one eye (general) or switching between eyes (swinging flashlight test)
- Abnormal light reflexes include (*see image below):
- Iridoplegia or mydriasis
- The involved oculomotor nerve is on the same side as the eye that remains dilated regardless of which eye is stimulated.
- Absolute afferent pupillary deficit (i.e., amaurotic pupil), or relative afferent pupillary deficit (aka, Marcus Gunn pupil)
- The affected optic nerve is on the same side as the eye that remains relatively dilated when directly illuminated (i.e., right eye remains dilated = right CN II involvement).
- Iridoplegia or mydriasis
TEST FOR ACCOMMODATION REFLEX
- Test procedure: Test with the convergence test.
-
Interpretation of results:
- Normal accommodation reflex = ocular ADduction and pupillary constriction of both eyes
- Abnormal accommodation reflex = ocular ADduction or pupillary constriction does not occur
- The involved optic or oculomotor nerve is on the same side as the eye that does not demonstrate ocular ADduction or pupillary constriction.
References:
- Nolan, pp.52-58
- Purves (6th ed.), pp.263-264
- For a review of the primary visual pathway, see Vander’s (15th ed.), Figure 7.31, p.213; Purves (6th ed.), Figure 12.3, p.265.
- For more information about visual quadrants, see Purves (6th ed.), pp.265-266 (“Retinotopic Representation of the Visual Field”)
- For more information about lens accommodation, see Purves (6th ed.), p.234, 236.
- NeuroLogic Exam: Cranial Nerve Exam (https://neurologicexam.med.utah.edu/adult/html/cranialnerve_normal.html#02)

Abnormal Light Reflexes
In the images below, light is shone in the right eye (i.e., the left eye in the image) to assess the light reflex. Determine (1) whether CN II or CN III is involved, and (2) what side the involved cranial nerve is on.

A: Oculomotor nerve, same side (i.e., right side)
B: Optic nerve, same side (i.e., right side)
C: Oculomotor nerve, opposite side (i.e., left side)
D: Optic nerve, opposite side (i.e., left side)
- This can also be a normal light reflex. If both pupils remain constricted when light is shone on the left eye, neither the optic nor oculomotor nerve is affected. However, if both pupils are dilated when light is shone on the left eye, the optic nerve on the opposite side is affected.

Visual Field Deficits
In the image showing visual field deficits, determine (1) what structure along the primary visual cortex is affected, and (2) which side the injury is on.

A: Injury to the RIGHT optic nerve prior to the optic chiasm = complete loss of vision (i.e., blindness) in the RIGHT eye
B: Injury at the optic chiasm = loss of temporal fields of vision in BOTH eyes
- Aka: Bitemporal hemianopsia, or heteromous hemianopsia
C: Injury at the optic tract on the RIGHT side = loss of the LEFT visual visual field in BOTH eyes (i.e., loss of the temporal field of the left eye, loss of nasal field of the right eye)
- Aka: Contralateral homonymous hemianopisa (i.e., loss of the visual field on the side opposite the lesion in the primary visual pathway)
- Example: In this case, injury at the right optic tract results in left homonymous hemianopsia.
D: Injury at the RIGHT optic radiation in the temporal lobe (aka, Meyer’s loop) = loss of the SUPERIOR portion of the LEFT visual field on BOTH sides (aka, left superior quadrantanopsia)
- Note: Injury at the RIGHT optic radiation in the parietal lobe (*not shown in the image) = loss of the INFERIOR portion of the LEFT visual field on BOTH sides (aka, left inferior quadrantanopsia)
E: Injury at the RIGHT primary visual cortex (aka, striate cortex) within the occipital lobe = LEFT homonymous hemianopsia with macular sparing
Reference:
- Purves (6th ed.), pp.263-264

CN III - Clinical Definition
What is cranial nerve III (i.e., CN III)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve III refers to the oculomotor nerve.
The oculomotor nerve emerges from the midbrain.
The oculomotor nerve contains motor fibers.
The oculomotor nerve is responsible for:
- Elevation of the superior eyelid
- Rotates the eyeball superiorly, inferiorly, and medially
- The oculomotor nerve innervates four of the six extraocular muscles: superior rectus, inferior rectus, medial rectus, and inferior oblique (*see image below).
- Constriction of the pupil
- Accommodation of the lens
References:
- Moore et al. (8th ed.), p.1072 (“Oculomotor Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), 62 (Table 5)
- For more information about actions of the extraocular muscles, see Purves (6th ed.), pp.448-450.

CN III - Etiology
What can cause injury to cranial nerve III (i.e., CN III)?
- Multiple sclerosis
- Myasthenia gravis
References:
- Coach K’s Lecture Materials –> Neuromuscular III
- Louis et al. (13th ed.), Section X: Demyelinating and Inflammatory Diseases (keyphrase: “Oculomotor abnormalities are common.”)
- Goodman and Fuller (4th ed.), p.1697 (“Myasthenia Gravis–Clinical Manifestations”)
CN III - Clinical Presentation
What are the hallmark signs and symptoms of injury to cranial nerve III (i.e., CN III)?
- Ptosis that does not resolve with upward gaze
- Dilated pupils
- Eyeball in a resting position of exotropia with hypotropia (“outward and down”) due to an unbalanced pull from the lateral rectus and superior oblique muscles (*see image below)
- Abnormal eye position may also be called “lateral strabismus.” See flashcard about heterotropia (aka, “strabismus”).
- Diplopia (double vision) with lateral gaze to the side opposite the affected oculomotor nerve
- Example: If the right oculomotor nerve was affected, attempting to look to the left will cause diplopia because the right eyeball will remain relatively unchanged from it’s resting position (see above) whereas the left eyeball will be ABducted (i.e., positioned laterally to the left).
References:
- Nolan, p.48
- Purves (6th ed.), pp.453-454

CN III - Special Tests
What is a special test or cluster of tests to rule in or rule out injury to cranial nerve III (i.e., CN III)?
- “H” test for extraocular movements (*see image below)
- Weakness or paralysis of one or more extraocular muscles results in heterotropia when the eyes move in the direction corresponding to the action of those muscles
- Example: Loss of motor control of right medial rectus muscle = heterotropia with diplopia with lateral gaze to the left
- Weakness or paralysis of one or more extraocular muscles results in heterotropia when the eyes move in the direction corresponding to the action of those muscles
- Light reflex and accommodation reflex tests (*see “CN II - Special Tests” flashcard)
Reference:
- Nolan, p.63,64 (Figure 7)























