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)
CN IV - Clinical Definition
What is cranial nerve IV (i.e., CN IV)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve IV refers to the trochlear nerve.
The trochlear nerve emerges from the midbrain.
The trochlear nerve contains motor fibers.
The trochlear nerve is responsible for rotating the eyeball inferiorly when the eyeball is ADducted (i.e., “inward and down”).
- The trochlear nerve innervates the superior oblique muscle of the eye.
*Note: The trochlear nerve is the only cranial nerve that innervates contralateral structures (e.g., the right trochlear nerve innervates the left superior oblique muscle of the eye).
References:
- Moore et al. (8th ed.), pp.1072-1073 (“Trochlear 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.
- NeuroLogic Examination: Cranial Nerve > Anatomy (https://neurologicexam.med.utah.edu/adult/html/cranialnerve_anatomy.html#01)
- Cranial Nerve: Functional Anatomy and Clinical Evaluation (http://vmerc.uga.edu/CranialNerves/trochlear.html)
CN IV - Etiology
What can cause injury to cranial nerve IV (i.e., CN IV)?
- Multiple sclerosis
- Myasthenia gravis
Reference:
- Goodman and Fuller (4th ed.), pp.1484-1485 (“Multiple Sclerosis–Clinical Manifestations”), 1697 (“Myasthenia Gravis–Clinical Manifestations”)
CN IV - Clinical Presentation
What are the hallmark signs and symptoms of injury to cranial nerve IV (i.e., CN IV)?
- Eyeball in a resting position of hypertropia and extorsion (i.e., “up and outward”) due to an unbalanced pull from the inferior oblique muscle
- Diplopia when attempting a downward gaze in the ADducted position with the affected eye
- Example: If the left trochlear nerve was affected, attempting to look to the left and downward 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) and rotated inferiorly.
- Head tilt to the side opposite the side of the affected eye (i.e., right eye involvement = left head tilt) to reduce symptoms of diplopia (*see image below)
Reference:
- Nolan, Table 7, p.71
What is a special test or cluster of tests to rule in or rule out injury to cranial nerve IV (i.e., CN IV)?
- “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 the right superior oblique muscle (i.e., left trochlear nerve involvement) = heterotropia with diplopia when attempting a downward gaze with the right eye ADducted (i.e., attempting to look to the left and downward)
- 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
Reference:
- Nolan, p.63,64 (Figure 7)
CN V - Clinical Definition
What is cranial nerve V (i.e., CN V)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve V refers to the trigeminal nerve.
The trigeminal nerve emerges from the pons.
The trigeminal nerve contains both sensory and motor fibers.
The trigeminal nerve is responsible for:
- Sensation from the face, cornea, and anterior tongue
- The skin on the face and scalp are innervated by the three divisions of the trigeminal nerve: ophthalmic (V1), maxillary (V2), and mandibular (V3) (*see image below).
- Muscles of mastication
- Masseter
- Temporalis
- Medial pterygoid
- Lateral pterygoid
References:
- Moore et al. (8th ed.), pp.1073-1074 (“Trigeminal Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), p.72
CN V - Etiology
What can cause injury to cranial nerve V (i.e., CN V)?
- Multiple sclerosis
- Trigeminal neuralgia is highly characteristic of multiple sclerosis in a young person.
- Myasthenia gravis
- In particular, myasthenia gravis can cause weakness and fatigability of the muscles of mastication.
Reference:
- Goodman and Fuller (4th ed.), p.1485 (Multiple Sclerosis–Clinical Manifestations), 1697 (“Myasthenia Gravis–Clinical Manifestations”)
Trigeminal Neuralgia - Clinical Definition
What is trigeminal neuralgia?
Trigeminal neuralgia (aka, tic douloureux) refers to severe electrical shock-like or stabbing pain that is strictly limited to the facial distribution of one or more divisions of the trigeminal nerve, or CN V: ophthalmic (V1), maxillary (V2), and mandibular (V3) (*see image below).
References:
- Louis et al. (13th ed.) (keyword: “trigeminal neuralgia”)
- Goodman and Fuller (4th ed.), p.1692
CN V - Clinical Presentation
What are the hallmark signs and symptoms of injury to cranial nerve V (i.e., CN V)?
- Sensory impairments of the face along the divisions of the trigeminal nerve
- Trigeminal neuralgia may be present.
- Impaired corneal reflex: No blinking of either eye when the cornea of the affected eye is touched, and blinking of both eyes when the cornea of the normal eye is touched
- Weakness of the muscles of mastication (i.e., masseter, temporalis, lateral pterygoid, medial pterygoid)
- If upper motor neuron pathways are involved, positive jaw-jerk reflex will be present.
*Note: See “CN V - Special Tests” flashcard for more details as well as references.
CN V - Special Tests
What is a special test or cluster of tests to rule in or rule out injury to cranial nerve V (i.e., CN V)?
SENSORY ASSESSMENT OF THE FACE
-
Test procedure: Use a safety pin to assess discrimination between sharp (painful) stimuli and blunt stimuli in the three divisions of the trigeminal nerve (*see below). Assess both sides of the face. The tested trigeminal nerve is on the same side being tested on the face (e.g., right trigeminal nerve = right side of the face).
- Ophthalmic (V1): Skin of the forehead above the eyebrows
- Maxillary (V2): Skin over the cheeks
- Mandibular (V3): Skin over the chin on each side of midline near the mental foramen
-
Interpretation of results
- Normal: Full sensation (sharp and blunt) on both sides of the face
-
Abnormal results on one or both sides of the face:
- Reduced sharp and blunt sensations (aka, hypoesthesia, hypesthesia)
- Reduced sharp (painful) sensation (aka, hypoalgesia)
- Increased sharp and blunt sensations (aka, hyperesthesia)
- Increased sharp (painful) sensation (aka, hyperalgesia)
- Perception of pain resulting from a stimuli that is not normally painful (aka, allodynia)
ASSESSEMENT OF CORNEAL REFLEX
- Test procedure: Ask the patient to direct his or her gaze to one side, keeping both eyes open. Approach the ADducted eye from the lateral side with a wisp of cotton that has been twisted to a point. Touch the cornea over the iris lateral to the pupil, taking care to avoid contacting the conjuctiva or sclera, or passing the cotton tip in front of the pupil. Repeat with the patient looking to the opposite side.
-
Interpretation of results
- Normal: Immediate blinking of both eyes, occasionally with movement of the head away from the stimulus
-
Abnormal:
- No blinking of either eye when the cornea of the affected eye is touched, and blinking of both eyes when the cornea of the normal eye is touched
- Due to injury of the ophthalmic division of the trigeminal nerve on the side of the affected eye
- When the cornea of the affected eye is touched, the affected eye does not blink whereas the normal eye does. When the cornea of the normal eye is touched, the affected eye remains open whereas the normal eye blinks.
- Due to injury of the facial nerve on the side of the affected eye
- No blinking of either eye when the cornea of the affected eye is touched, and blinking of both eyes when the cornea of the normal eye is touched
ASSESSMENT OF MUSCLES OF MASTICATION
-
Masseter, temporalis, and medial pterygoid
- Test procedure: Ask the patient to close the mouth and gently approximate the teeth. Palpate the masseter and temporalis muscles of both sides of the face as the patient bites hard.
-
Interpretation of results:
- Normal: Equal and symmetric contractions of the masseter and temporalis; jaws cannot be separated when pushing down on the chin
-
Abnormal: Unequal or asymmetric contractions of the masseter or temporalis
- Due to injury of the trigeminal nerve on the side of the affected muscle of mastication
-
Lateral pterygoid
- Test procedure: Ask the patient to push the jaw forward with the mouth slightly open.
-
Interpretation of results:
- Normal: The jaw moves straight forward approximately 1 cm.
-
Abnormal: Deviation of the jaw to one side
- Due to injury of the trigeminal nerve on the same side of the jaw deviation (e.g., deviation of the jaw to the right = injury to the right trigeminal nerve)
JAW JERK REFLEX
- Test procedure: Have the patient slightly open their mouth. Then place your finger on their chin and strike your finger with a reflex hammer.
-
Interpretation of results
- Normal: No movement
- Abnormal: Brisk movement of the jaw upward as the mouth closes; may be indicative of an upper motor neuron problem
References:
- Nolan, pp.74-77
- NeuroLogic Exam: Cranial Nerve > Normal (https://neurologicexam.med.utah.edu/adult/html/cranialnerve_normal.html#16)
- For more information about the jaw-jerk reflex, see ScienceDirect: Jaw-Jerk Reflex (https://www.sciencedirect.com/topics/medicine-and-dentistry/jaw-jerk-reflex).
CN VI - Clinical Definition
What is cranial nerve VI (i.e., CN VI)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve VI refers to the abducens (abducent) nerve.
The abducens nerve emerges from the pons.
The abducens nerve contains motor fibers.
The abducens nerve is responsible for rotating the eye outward.
- The abducens nerve innervates the lateral rectus muscle of the eye.
References:
- Moore et al. (8th ed.), p.1074 (“Abducent Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), 62 (Table 5)
CN VII - Clinical Definition
What is cranial nerve VII (i.e., CN VII)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve VII refers to the facial nerve.
The facial nerve emerges from the pons.
The facial nerve contains both sensory and motor fibers.
The facial nerve is responsible for:
- Taste from anterior two-thirds of the tongue
- Muscles of facial expression, including:
- Frontalis
- Orbicularis oculi
- Zygomaticus major
- Orbicularis oris
- Tearing (lacrimal) glands
- Salivary glands
References:
- Moore et al. (8th ed.), pp.1076-1077 (“Facial Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), 83
CN VII - Etiology
What can cause injury to cranial nerve VII (i.e., CN VII)?
- Multiple sclerosis
- Amyotrophic lateral sclerosis (ALS)
- Myasthenia gravis
- Bell’s palsy
Reference:
- Goodman and Fuller (4th ed.), p.1485 (“Multiple Sclerosis–Clinical Manifestations”), 1457 (“Amyotrophic Lateral Sclerosis–Clinical Manifestations”), 1697 (“Myasthenia Gravis–Clinical Manifestations”)
Bell’s Palsy - Clinical Definition
What is Bell’s palsy?
Bell’s palsy (aka, Bell palsy, idiopathic facial paralysis) refers to acute, unilateral paresis or paralysis of all of the muscles innervated by the facial nerve (CN VII) that appears spontaneously, over hours to days. Other associated signs and symptoms include dry eyes (i.e., decreased tearing), dry mouth (i.e., decreased salivation), dysarthria, impaired taste on the anterior two-thirds of the tongue on the affected side, and a weakened or absent corneal reflex (i.e., minimal to no blinking of the affected eye when the cornea of either eye is touched).
In contrast, an upper motor neuron lesion (e.g., following a middle cerebral artery stroke) will result in weakness of only the inferior facial muscles on the contralateral side.
References:
- Louis et al. (13th ed.) (keyword: Bell palsy)
- Purves (6th ed.), p.385 (“Clinical Applications”)
Bell’s Palsy - Interventions
What physical therapy interventions are utilized to treat Bell’s palsy?
Electrical stimulation of the facial muscles of expression
CN VII - Clinical Presentation
What are the hallmark signs and symptoms of injury to cranial nerve VII (i.e., CN VII)?
- See “Bell’s Palsy - Clinical Definition”
- Inability to completely close one or both eyes (i.e., lagophthalmos) can result in an observable Bell phenomenon
References:
- Nolan, p.84
Bell Phenomenon
What is Bell phenomenon?
Bell phenomenon is a defensive reflex mechanism characterized by the upward and inward deviation of the affected eye (i.e., eye supraduction) when attempting to close that eye. Normally, Bell phenomenon helps to keep the eye moist and protected during eye closure. Bell phenomenon is observable when closure of the eyelid is incomplete, and an observable Bell phenomenon is associated with injury to the facial nerve (CN XII).
References:
- Nolan, p.82
- Louis (13th ed.) (keyword: Bell phenomenon)
- ScienceDirect: Bell’s Phenomenon (https://www.sciencedirect.com/topics/medicine-and-dentistry/bells-phenomenon)
CN VII - Special Tests
What is a special test or cluster of tests to rule in or rule out injury to cranial nerve VII (i.e., CN VII)?
ASSESSEMENT OF CORNEAL REFLEX
- See “CN V - Special Tests” flashcard.
ASSESSMENT OF MUSCLES OF FACIAL EXPRESSION
-
Test procedure: Ask the patient to perform the following movements associated with the actions of the muscles of facial expression.
- Orbicularis oris: “Purse or pucker your lips as if whistling or kissing.”
- Zygomaticus major: “Smile widely, and show your teeth.”
- Orbicularis oculi: “ Close your eyes tightly.”
- Frontalis: “Raise the eyebrows.”
-
Interpretation of results
-
Normal
- Frontalis: The eyebrows rise, producing wrinkles in the forehead.
- Orbicularis oculi: Eye closure is symmetric; equal strength (i.e., resistance) when attempting to gently pry the eyes open
- Zygomaticus major: Both corners of the mouth move laterally upon smiling; smile is symmetrical
- Orbicularis oris: Lips on both sides of the face come together upon pursing or puckering the lips
-
Abnormal: Asymmetrical or absent facial expressions
- In asymmetrical facial expressions, the involved facial nerve is on the same side as the affected side of the face.
-
Normal
ASSESSMENT OF TASTE
- Test procedure: Ask the patient to stick out his or her tongue. Using a cotton applicator moistened with the test solution, apply dilute solutions of glucose (sweet), sodium chloride (salty), citric acid (sour), quinine (bitter), and water (i.e., control stimulus) to either side of the tongue separately. Ask the patient to indicate what he or she is tasting by pointing to one of the given cards with the following labels: SWEET, SALTY, SOUR, BITTER, and WATER.
-
Interpretation of results:
- Normal: Patient is able to correctly identify each test solution.
-
Abnormal:
- Absence of taste (i.e., ageusia)
- Decreased taste sensation (i.e., hypogeusia)
Reference:
- Nolan, pp.82-83
CN VIII - Clinical Definition
What is cranial nerve VIII (i.e., CN VIII)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve VII refers to the vestibulocochlear (auditory) nerve.
The vestibulocochlear nerve emerges from the pons.
The vestibulocochlear nerve contains special sensory fibers.
The vestibulocochlear nerve is responsible for balance (semicircular canals, utricle, saccule) and hearing (organ of Corti).
References:
- Moore et al. (8th ed.), pp.1078-1079 (“Vestibulocochlear Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4)
CN IX - Clinical Definition
What is cranial nerve IX (i.e., CN IX)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve IX refers to the glossopharyngeal nerve.
The glossopharyngeal nerve emerges from the medulla oblongata.
The glossopharyngeal nerve contains both sensory and motor fibers.
The glossopharyngeal nerve is responsible for:
- Taste for the posterior one-third of the tongue
- Sensation for posterior tongue and oropharynx
- Salivary gland
- Conveying impulses from the baroreceptors in the carotid sinus
References:
- Moore et al. (8th ed.), pp.1079-1080 (“Glossopharyngeal Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), 96
CN X - Clinical Definition
What is cranial nerve X (i.e., CN X)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve X refers to the vagus nerve.
The vagus nerve emerges from the medulla oblongata.
The vagus nerve contains both sensory and motor fibers.
The vagus nerve is responsible for:
- Muscles of the larynx (for phonation), pharynx, and soft palate
References:
- Moore et al. (8th ed.), pp.1081-1083 (“Vagus Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), 62 (Table 5)
CN IX and CN X- Etiology
What can cause injury to cranial nerves IX and X (i.e., CN IX and CN X)?
- Amyotrophic lateral sclerosis (ALS)
- Lateral medullary (Wallenberg) syndrome secondary to infarction of the lateral medulla and posteroinferior cerebellum
- Characterized by vertigo, ipsilateral ataxia, Horner syndrome (due to damage of descending sympathetic fibers), impairment of sensation in the ipsilateral portion of the face and contralateral portion of the torso and limbs, and dysphagia
- Myasthenia gravis
- In particular, weakness and fatigability of the palatal and pharyngeal muscles due to impairment of the vagus nerve can result in dysphagia.
References:
- Goodman and Fuller (4th ed.), p.1457 (“Amyotrophic Lateral Sclerosis–Clinical Manifestations”), 1516 (“Vertebral and Posterior Inferior Cerebellar Artery Syndrome”), 1697 (“Myasthenia Gravis–Clinical Manifestations”)
- Medscape: Vertebrobasilar Artery Stroke Syndromes (https://emedicine.medscape.com/article/323409-overview#a7)
CN IX and CN X - Clinical Presentation
What are the hallmark signs and symptoms of injury to cranial nerves IX and X (i.e., CN IX and CN X)?
Specific to vagus nerve:
- Dysphonia (i.e., a change in voice quality in which the voice sounds hoarse)
- Abnormal deviation of the uvula at rest or during phonation
Specific to both the glossopharyngeal and vagus nerves:
- Dysphagia
- Note that dysphagia can also indicate involvement of the trigeminal nerve, facial nerve, or hypoglossal nerve.
- Abnormal gag reflex
*Note: See “CN IX and CN X - Special Tests” for more information and references.
CN IX and CN X - Special Tests
What is a special test or cluster of tests to rule in or rule out injury to cranial nerves IX and X (i.e., CN IX and CN X)?
ASSESSMENT OF SWALLOWING
-
Test procedure: Have the patient drink a glass of water and report his or her ease with swallowing.
- Assessment of swallowing examines both the glossopharyngeal and vagus nerves. Note that three other cranial nerves are involved in the action of swallowing: trigeminal nerve, facial nerve, and hypoglossal nerve.
-
Interpretation of results:
- Normal: Swallowing is free and unhindered.
- Abnormal: Swallowing is difficult (i.e., dysphagia).
ASSESSEMENT OF UVULA AND SOFT PALATE
-
Test procedure: With the patient’s mouth open and the tongue kept relaxed on the floor of the mouth, assess the shape and resting position of the uvula. Then have the patient say, “Ah,” and observe the movement of the uvula and soft palate during phonation.
- Assessment of the uvula and soft palate primarily examines the vagus nerve.
-
Interpretation of results
-
Normal:
- At rest, the uvula is symmetric in shape and located essentially in the middle of the mouth.
- During phonation, there is symmetric elevation of the soft palate without movement of the uvula in either direction.
-
Abnormal:
- At rest, there is a grossly apparent asymmetry of the soft palate or deviation of the uvula.
- During phonation, inability to elevate the soft palate on the involved results in deviation of the uvula away from the affected side (e.g., deviation of the uvula to the left = right vagus nerve involvement)
-
Normal:
ASSESSMENT OF GAG REFLEX
-
Test procedure: With the mouth open, gently touch the lateral pharyngeal wall of one side with a tongue depressor or a cotton-tipped applicator. Repeat with the other side.
- Assessment of the gag reflex examines both the glossopharyngeal and vagus nerves.
-
Interpretation of results:
- Normal: Strong contraction of the upper pharyngeal muscles (gagging)
-
Abnormal:
- Normal gag reflex with stimulation of the normal side, and loss of gag reflex with stimulation on the involved side
- Due to injury of the glossopharyneal nerve on the involved side
- Absent gag reflex with stimulation on both sides
- Involvement of both the glossopharyngeal and vagus nerves, OR…
- Possibly due to aging process with no involvement of the glossopharyngeal or vagus nerves
- Normal gag reflex with stimulation of the normal side, and loss of gag reflex with stimulation on the involved side
Reference:
- Nolan, pp.100-101
CN XI - Clinical Definition
What is cranial nerve XI (i.e., CN XI)?
Where does it enter or emerge?
What type of functional fibers does it contain?
What is it’s function?
Cranial nerve X refers to the spinal accessory nerve.
The spinal accessory nerve emerges from the medulla oblongata.
The spinal accessory nerve contains motor fibers.
The spinal accessory nerve is responsible for innervating the sternocleidomastoid and trapezius (upper, middle, lower) muscles.
References:
- Moore et al. (8th ed.), p.1083 (“Spinal Accessory Nerve”)
- Purves et al. (6th ed.), pp.A-8 to A-9 (Table A2)
- Nolan, p.44 (Table 4), 62 (Table 5)
Common Eye Disorders
Determine whether the following eye conditions are ones that describe visual acuity deficits or visual field deficits:
- Cataracts
- Macular degeneration
- Glaucoma
Cataracts and macular degeneration reflect visual acuity deficits. Cataracts refers to opacities in the lens of the eye (i.e., “clouding of the lens”) that results in a loss of transparency in that lens. Macular degeneration (aka, age-related macular degeneration) refers to a loss of central vision due to damage to the macula lutea, a region of the retina that supports high visual acuity.
- The loss of visual acuity associated with cataracts or macular degeneration only affects the eye of origin (e.g., cataracts of the right eye = right eye involvement).
Glaucoma reflects a visual field deficit. Glaucoma refers to a loss of peripheral vision due to inadequate drainage of the eye’s aqueous humor that leads to increased intraocular pressure, reduced blood supply to the eye, and eventual damage to the retinal neurons.
- The loss of visual field associated with glaucoma only affects the eye of origin (e.g., glaucoma of the right eye = right eye involvement).
Reference:
- Purves (6th ed.), p.234, 237 (“Clinical Applications: Macular Degeneration”), 263 (“Clinical Applications: Visual Field Deficits” [“Damage to the retina or to one of the optic nerves…”])
Tenodesis Action
What is the tenodesis action?
Tenodesis action refers to the automatic and passive flexion of the fingers and thumbs that is produced when the extrinsic flexors of the digits of the hand (i.e., flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus) are stretched in a position of wrist extension (*see image below).
Reference:
- Neumann (3rd ed.), p.274 (“Passive Finger Flexion via ‘Tenodesis Action’ of the Extrinsic Digital Flexors”
Babinski Sign and Hoffmann Sign
What is the Babinski sign and Hoffman sign? How is each tested, and what does each indicate?
The Babinski sign (*see image below) refers to the atypical fanning of the toes and the extension of the big toe when stroking the sole of the foot.
- In adults, the Babinski sign is associated with damage to the corticospinal tract.
- In infants before the maturation of the corticospinal pathway, the Babinski sign occurs as a result of the incomplete upper motor neuron control of local motor neuronal circuitry.
Hoffmann sign is the upper extremity equivalent of the Babinski sign and, if present in adults, also indicates damage along the corticospinal tract. The Hoffmann sign is characterized by flexion or ADduction of the 1st interphalangeal (IP) joint of the thumb as well as flexion of the fingers when the distal phalanx of the middle finger is flicked briskly.
References:
- Purves (6th ed.), p.403
- Magee (6th ed.), p.200
- Physiopedia: Hoffmann’s Sign (https://physio-pedia.com/Hoffmann%27s_Sign#:~:text=A%20positive%20Hoffmann%27s%20sign%20is%20suggestive%20of%20corticospinal,anxiety%20will%20also%20result%20in%20a%20positive%20sign.)
UE Dermatomes
Name the area of skin along the upper extremity supplied by the following spinal nerves:
- C5
- C6
- C7
- C8
- T1
- C5: Anterior deltoid region
- C6: Thumb
- C7: Middle finger
- C8: Ulnar aspect of forearm
- T1: Medial aspect of upper arm
Reference:
- See neuroscreening lecture from ECS I.
LE Dermatomes
Name the area of skin along the lower extremity that is supplied by the following dermatomes:
- L2
- L3
- L4
- L5
- S1
- L2: Proximal aspect of the anterior thigh
- L3: Middle of the anterior thigh to the medial aspect of the knee
- L4: Medial aspect of the lower leg
- L5: Proximal aspect of the lateral lower leg, or the dorsum of foot between the great toe and second toe
- S1: Lateral surface of the foot
Reference:
- See neuroscreening lecture from ECS I.
SCI - ASIA Impairment Scale
Describe how spinal cord injuries (SCI) are classified based on the various levels associated with the ASIA impairment scale.
Classifications of spinal cord injuries can be determined using the American Spinal Cord Injury Association (ASIA) Impairment Scale (or AIS).
-
A (complete SCI):
- No preservation of motor and sensory functions in the lowest sacral segments (S4-S5) (i.e., no sacral sparing)
-
B (sensory incomplete SCI):
- Sensory but not motor function is preserved below the neurological level of injury
- Includes preservation of only sensory function at the lowest sacral segments (S4-S5) (i.e., sparing of sacral sensation, including light touch or pin prick at S4-S5 or deep anal pressure)
- No motor function is preserved more than three levels below the motor level on either side of the body
- Motor level is defined as the lowest segment representing key muscle function that has a grade of at least 3 (on supine testing), providing that the key muscle functions represented by segments above that motor level are judged to be intact (i.e., graded as a 5) (*see image below).
- Sensory but not motor function is preserved below the neurological level of injury
-
C (motor incomplete SCI):
- Motor function is preserved below the neurological level of injury
- Less than half of the key muscle functions below the neurological level of injury have a muscle grade greater than or equal to 3
-
D (motor incomplete SCI):
- Motor function is preserved below the neurological level of injury
- At least half (half or more) of key muscle functions below the neurological level of injury have a muscle grade greater than or equal to 3
-
E (normal):
- If tested sensation and motor functions are graded as normal in all segments, and the patient had prior deficits associated with SCI, then the AIS grade is E. Someone without an initial SCI does not receive an AIS grade.
References:
- Goodman and Fuller (4th ed.), p.1561 (“Clinical Manifestations–Level of Injury”)
- O’Sullivan et al. (7th ed.), p.859 (“ASIA Impairment Scale;” Box 20.1)
Brown-Séquard Syndrome - Clinical Presentation
What is Brown-Séquard syndrome?
Brown-Séquard syndrome refers to a collection of signs and symptoms associated with an incomplete spinal cord injury characterized by damage to one side (i.e., hemisection) of the spinal cord, often due to stabs or gunshot wounds. The most common presentation is the Brown-Séquard plus syndrome, which is characterized by ipsilateral hemiplegia and hemianesthesia with contralateral hemianalgesia.
The hallmark signs and symptoms of Brown-Séquard syndrome include (*see also image below):
-
Ipsilateral side of the lesion
- Lateral corticospinal symptoms: Weakness, brisk reflexes with clonus, positive Babinski sign, spasticity
- Dorsal column-medial lemniscal symptoms: Loss of proprioception, vibration, tactile discrimination
- Zone of complete loss of sensation due to overlap of anterolateral symptoms with dorsal column-medial lemniscal symptoms (*see below)
-
Contralateral side of the lesion
- Anterolateral (i.e., spinothalamic) symptoms: Loss of pain and temperature
- Initially presents as an ipsilateral loss that occurs several dermatome segments below the neurological level of injury and then is followed by contralateral loss below those dermatome segments
- Anterolateral (i.e., spinothalamic) symptoms: Loss of pain and temperature
References:
- Purves et al. (6th ed.), pp.217-218, Figure 10.4; 385-386
- O’Sullivan et al. (7th ed.), p.860 (Brown-Séquard Syndrome)
- Goodman and Fuller (4th ed.), p.1561 (“Spinal Cord Injury Syndromes”), 1563 (Figure 34.10)
- Louis et al. (13th ed.) (keyword: Brown-Séquard Syndrome)
Central Cord Syndrome - Clinical Presentation
What is central cord syndrome?
Central cord syndrome is a collection of signs and symptoms associated with an incomplete spinal cord injury characterized by damage to the central aspects of the spinal cord, often due to cervical hyperextension injuries. Central cord syndrome is the most common incomplete SCI syndrome.
The hallmark signs and symptoms of central cord syndrome include (*see image below):
- Loss of motor function that is greater in the upper extremities than the lower extremities
- Varying degrees of sensory impairment occur but tend to be less severe than motor deficits.
References:
- Goodman and Fuller (4th ed.), p.1563 (“Central Cord Syndrome”)
- O’Sullivan et al. (7th ed.), p.860 (“Central Cord Syndrome”)
Anterior Cord Syndrome - Clinical Presentation
What is anterior cord syndrome?
Anterior cord syndrome is a collection of signs and symptoms associated with an incomplete spinal cord injury characterized by damage to the anterior and anterolateral aspects of the spinal cord, often due to flexion injuries.
The hallmark signs and symptoms of anterior cord syndrome include (*see image below):
- Bilateral loss of motor function
- Bilateral loss of pain and temperature sensation
References:
- Goodman and Fuller (4th ed.), p.1563 (“Anterior Cord Syndrome”)
- O’Sullivan et al. (7th ed.), p.860 (“Anterior Cord Syndrome”)
Posterior Cord Syndrome - Clinical Presentation
What is posterior cord syndrome?
Posterior cord syndrome is a collection of signs and symptoms associated with an incomplete spinal cord injury characterized by damage to the posterior aspect of the spinal cord, which can occur as a result of hyperextension. Posterior cord syndrome is extremely rare.
The hallmark signs and symptoms of posterior cord syndrome include (*see image below):
- Preservation of motor function, pain, and light touch sensation
- Loss of proprioception, kinesthesia, two point discrimination, stereognosis (aka, tactile agnosia)
- Loss of proprioception and kinesthesia can result in severe gait deviations.
References:
- Goodman and Fuller (4th ed.), p.1563 (“Posterior Cord Syndrome”)
- Louis et al. (13th ed.) (keyword: “Posterior Cord Syndrome”)
Myasthenia Gravis - Special Test
What is a special test or cluster of tests to rule in or rule out myasthenia gravis?
The ice test for myasthenia gravis (*see also image below):
- A pack of ice is placed over the eye demonstrating ptosis for 1 to 2 minutes.
- Resolution or improvement in the ptosis is considered positive and highly specific for myasthenia gravis.
- It is unclear why decreased temperature reduces ptosis, but a proposed hypothesis is that decreased temperatures improves neuromusclar transmission.
References:
- Louis et al. (13th ed.) (keyword: ice test)
- SpringerLink: Ice Pack Test for Myasthenia Gravis (https://link.springer.com/referenceworkentry/10.1007/978-3-642-35951-4_1285-1)
- BMJ: Can myasthenia gravis…? (https://pmj.bmj.com/content/76/893/162)
Sciatica
What is sciatica?
How is sciatica tested?
Sciatica refers to pain radiating from the lower back into the buttock and down the posterior or lateral aspect of the thigh into the leg. Sciatica is often caused by a herniated lumbar intervertebral disc that compresses and compromises the L5 or S1 component of the sciatic nerve.
-
Note: Posterior or posterolateral protrusions at the L4-L5 and L5-S1 levels are most common types of herniated intervertebral discs (*from Kisner and Colby [7th ed.], p.446 [“Variability of symptoms”]). The general rule is that when an herniated intervertebral disc protrudes posterolaterally, it usually compresses the spinal nerve numbered one inferior to the herniated disc. For example, a L4–L5 herniated intervertebral disc compresses the L5 spinal nerve, and a L5-S1 herniated intervertebral disc compresses the S1 spinal nerve (*from Moore et al. [8th ed.], p.109).
- See also Netter Plate 161 (PDF p. 187) for a visual example of a herniated intervertebral disc and its effect on nearby spinal nerves.
- Posterolateral protrusions at the lumbar spine are usually treated with lumbar extension exercises to help mechanically reduce the protrusion and cause centralization of the pain (*from Kisner and Colby [7th ed.], p.447 [“Objective Clinical Findings in the Lumbar Spine”]).
Any maneuver that stretches the sciatic nerve, such as extending the knee (e.g., sitting knee extension) or flexing the thigh with the knee extended (e.g., straight leg-raise test in supine), generally produces or exacerbates sciatica.
-
Straight-leg raise test (*see image below)
- Procedure: With the patient in supine, passively flex the hip of the affected lower extremity while keeping the knee extended.
-
Positive results for sciatica:
- Neurological symptoms (e.g., burning, tingling, shooting) that occur below the gluteal fold and between 30-50° of hip flexion
- Neurological symptoms become worse or more peripheral (i.e., below the gluteal cleft) when passively dorsiflexing the ankle of the affected lower extremity at the patient’s limit of the straight-leg raise motion.
References:
- Moore et al. (8th ed.), p.109
- See ECS I lecture, “Neuroscreening” (p.15)
CTS - Clinical Definition
What is carpal tunnel syndrome (CTS)?
Carpal tunnel syndrome (CTS) (aka, median neuropathy, tardy median palsy) refers to compression of the median nerve within the carpal tunnel in the wrist that results in pain, paresthesia, numbness, and weakness in the distribution of the median nerve.
- The carpal tunnel is a osseofibrous passageway at the wrist through which the median nerve, flexor pollicis longus tendon, flexor digitorum superficialis tendons, and flexor digitorum profundus tendons pass through (*see image below). The hallmark of the carpal tunnel is that it is cylindrical and inelastic. None of the sides of the tunnel yields to expansion of the fluid or structures within. Change within the tunnel is the basis of study related to the etiology of carpal tunnel, but the matrix of possible causes proves to be complex and not fully understood at this time.
Reference:
- Goodman and Fuller (4th ed.), p.1668 (“Median Neuropathy: Carpal Tunnel Syndrome”), 1668-1669 (“Etiology”)
CTS - Clinical Presentation
What are the hallmark signs and symptoms of carpal tunnel syndrome (CTS)?
- Sensory symptoms in the median nerve distribution (*see image below)
- Nocturnal pain
- Pain may be located distally in the forearm or wrist and radiate into the thumb, index, and middle fingers. Pain may also radiate into the arm, shoulder, and neck.
- Decreased two-point discrimination, vibration, pressure, and light touch
- Muscle atrophy and motor symptoms can develop in advanced cases of CTS.
Reference:
- Goodman and Fuller (4th ed.), p.1670 (“Clinical Manifestations”)
CTS - Special Tests
What is a special test or cluster of tests to rule in or rule out carpal tunnel syndrome (CTS)?
-
Tinel’s sign
- Procedure: The examiner taps over the carpal tunnel at the wrist.
-
Interpretation: A positive result is characterized by tingling or paresthesia into the thumb, index finger (forefinger), and middle and lateral half of the ring finger (median nerve distribution). The tingling or paresthesia is felt distal to the point of pressure.
- Indicates carpal tunnel syndrome
-
Nerve conduction velocity test
- A nerve conduction velocity test (*see image below) measures the speed at which an electrical stimulus passes through the nerves. Latency, or the time it takes for the electrical impulse to travel from the stimulation site to the recording site, is measured. Increased latency is associated with conditions involving damage to nerves (e.g., carpal tunnel syndrome).
References:
- Magee (6th ed.), p.474 (“Tinel Sign [at the Wrist]”)
- JCDR: The Comparision of the Motor Nerve Conduction Velocity (https://www.jcdr.net/article_fulltext.asp?id=1195#:~:text=INTRODUCTION.%20The%20nerve%20conduction%20study%20%28NCS%29%20is%20a,motor%20and%20sensory%20nerves%20of%20the%20human%20body.)
LE Myotomes
Name the primary muscles, peripheral nerves, and spinal nerves associated with each muscle action:
- Hip flexion
- Hip extension
- Hip ABduction
- Knee flexion
- Knee extension
- Ankle dorsiflexion
- Ankle plantarflexion
- Ankle eversion
- Ankle inversion
-
Hip flexion
-
Iliopsoas muscle group
-
Psoas major:
- Peripheral innervation: Anterior primary rami of L1, L2, and L3 spinal nerves
- Segmental innervation: L1, L2, L3, and L4 spinal nerves
-
Iliacus:
- Peripheral innervation: Femoral nerve
- Segemental innervation: L1, L2, L3, L4 spinal nerves
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Psoas major:
-
Iliopsoas muscle group
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Hip extension
-
Gluteus maximus
- Peripheral innervation: Inferior gluteal nerve
- Segmental innervation: L5, S1, and S2 spinal nerves
-
Gluteus maximus
-
Hip ABduction
-
Gluteus medius and gluteus minimus
- Peripheral innervation: Superior gluteal nerve
- Segmental innervation: L4, L5, and S1 spinal nerves
-
Gluteus medius and gluteus minimus
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Knee flexion
-
Hamstrings muscle group
-
Semimembranosus
- Peripheral innervation: Tibial nerve
- Segmental innervation: L4, L5, S1, and S2 spinal nerves
-
Semitendinosus
- Peripheral innervation: Tibial nerve
- Segmental innervation: L4, L5, S1, and S2 spinal nerves
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Biceps femoris (long head)
- Peripheral innervation: Tibial nerve
- Segmental innervation: L5, S1, S2, and S3 spinal nerves
-
Biceps femoris (short head)
- Peripheral innervation: Common fibular (peroneal) nerve
- Segmental innervation: L5, S1, and S2 spinal nerves
-
Semimembranosus
-
Hamstrings muscle group
-
Knee extension
-
Quadriceps femoris muscle group: Rectus femoris, vastus medialis, vastus lateralis, vastus intermedius
- Peripheral innervation: Femoral nerve
- Segmental innervation: L2, L3, and L4 spinal nerves
-
Quadriceps femoris muscle group: Rectus femoris, vastus medialis, vastus lateralis, vastus intermedius
-
Ankle dorsiflexion
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Tibialis anterior, extensor hallucis longus, extensor digitorum longus
- Peripheral innervation: Deep fibular (peroneal) branch of the common fibular nerve
- Segmental innervation: L4, L5, and S1 spinal nerves
-
Tibialis anterior, extensor hallucis longus, extensor digitorum longus
-
Ankle plantarflexion
-
Triceps surae muscle group
-
Gastrocnemius
- Peripheral innervation: Tibial nerve
- Segmental innervation: S1 and S2 spinal nerves
-
Soleus
- Peripheral innervation: Tibial nerve
- Segmental innervation: L5, S1, and S2 spinal nerves
-
Gastrocnemius
-
Tibialis posterior
- Peripheral innervation: Tibial nerve
- Segmental innervation: L4, L5, and S1 spinal nerves
-
Triceps surae muscle group
-
Ankle eversion
-
Fibularis longus and brevis
- Peripheral innervation: Superficial fibular (peroneal) branch of the common fibular nerve
- Segmental innervation: L4, L5, and S1 spinal nerves
-
Fibularis longus and brevis
-
Ankle inversion
- Tibialis posterior (*see above)
-
Flexor digitorum longus; flexor hallucis longus
- Peripheral innervation: Tibial nerve
- Segmental innervation: L5, S1, and S2 spinal nerves
