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Neuro Flashcards

Neuro portions of the exam

1
Q

Lateral spinothalamic tract
Which category?
Role?
Where it crosses?
How to test?

A

Category: Ascending tract, SENSORY
Role: Pain and temperature
Where it crosses: Within spinal cord at level of innervation
How to test: Sharp/dull, hot/cold

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2
Q

Anterior spinothalamic
Which category?
Role?
Where it crosses?
How to test?

A

Category: Ascending tract, SENSORY
Role: Pressure and crude touch
Where it crosses: Within spinal cord at level of innervation
How to test: Light touch

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3
Q

Dorsal column (medial lemniscus)
Which category?
Role?
Where it crosses?
How to test?

A

Category: Ascending tract, SENSORY
Role: Proprioception, deep touch, discrimination, vibration, stereognosis
Where it crosses: pyramid motor (medulla) in brain stem, contralateral effected
How to test: tuning fork, 2 pt discrimination, kinesthesia, proprioception, stereognosis

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4
Q

Lateral corticospinal
Which category?
Role?
Where it crosses?
How to test?

A

Category: Descending tract, MOTOR
Role: MAIN motor path, motor fxn of limbs and digits musculature
Where it crosses: pyramid motor (medulla) in brain stem
How to test: Injury would result in UMNL presentation (hyperreflexia)

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5
Q

Anterior corticospinal
Which category?
Role?
Where it crosses?
How to test?

A

Category: Descending tract, MOTOR
Role: motor fxn for posture and axial musculature
Where it crosses: within spinal cord at level of innervation
How to test: no specific tests

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6
Q

Corticorubrospinal tract
What category?
Role?

A

Category: Descending, MOTOR
Role: similar to corticospinal (back up system)

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7
Q

Corticoreticulospinal tract
What category?
Role?

A

Category: Descending tract, MOTOR
Role: posture and locomotion, automatic functions (respiration, circulation, sweating, shivering, dilation, sphincteric muscles)

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8
Q

Vestibulospinal tract
What category?
Role?

A

Category: Descending tract, MOTOR
Role: Postural reactions, standing balance

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9
Q

Traumatic spinal cord injuries
Stats, how they occur

A

40% are cervical incomplete
Tetra and paraplegic common
MOI: hyperflexion, hyperextension, axial load, penetrating injuries, falls, transportation

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10
Q

Non-traumatic spinal cord injury causes

A

Cancer, infection, inflammation, motor neuron disorders, vascular diseases (spinal cord infarcts)
Most are paraplegic

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11
Q

Spinocerebellar tract
What category?
Role?
Crossing?

A

Category: Ascending, SENSORY
Role: non-conscious proprioception (walking)
Crossing: some crossed and some uncrossed (4 total tracts)

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12
Q

Spinal Cord Immediate Treatment
Goals

A

Prevent edema by using ice to reduce the chance of secondary injury (ischemia, hypoxia, necrosis)
Immobilized
Manage airways, breathing, circulation, injuries
Surgery: if need alignment changes, stabilization, reduce medical complications

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13
Q

Level of lesion

A

Most caudal segment of the spinal cord with normal sensory and motor function on both sides of the body

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14
Q

Motor level of ASIA scale

A

Most caudal segment with a grade >/= 3 with ALL segments above being grade 5
If T2-L1 then determined by intact sensory segment level

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15
Q

Sensory level of ASIS scale

A

Most caudal segment with bilateral score of 2 for both light touch and pin prick
Graded by 0 = absent, 1 = impaired, 2 = normal

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16
Q

ASIA A

A

No sensory or motor function is preserved in the sacral segments (S4-5)

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17
Q

ASIA B

A

Sensation but NOT motor is preserved below the neurological level and includes sacral segments

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18
Q

ASIS C = sensory incomplete

A

More than half of the key muscles below the NLI have a grade 3 or less

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19
Q

ASIS D = motor incomplete

A

More than half of the key muscles below the NLI have grade 3 or equal to 3

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20
Q

ASIA E = normal

A

Normal sensory and motor function
Uses with patients who have prior history of SCI

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21
Q

Deep anal pressure = what ASIA?

A

If present, ASIA B (sensory incomplete)

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22
Q

Voluntary Anal Pressure = what ASIA?

A

If present, ASIA C (motor incomplete)

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23
Q

Zone of Partial Preservation (ZPP)

A

Might be dermatomes present below sensory level and myotomes below motor level that remain partially innervated
Most caudal segment with sensory defines extent of ZPP
ONLY FOR ASIA A

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24
Q

Pin prick prognostication

A

Pin prick (LE and sacral) within 72 hours is good indicator of motor function and ability to walk

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25
Q

Central cord syndrome

A

Most common
Damage to central cord
Hyperextension of neck, usually in elderly who fall
More loss in UE than LE
Associated with spinal canal stenosis

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26
Q

Brown Sequard Syndrome

A

Compression of one side of the spinal cord or hemisection
Typically seen after knife/penetrating injury
ISPILATERAL loss of motor
CONTRALATERAL loss of sensation

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27
Q

Anterior Cord Syndrome

A

Rare
Occlusion of blood supply to the anterior cord (pain and temperature) below injury level

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28
Q

Conus Medullaris Syndrome

A

Conus medullaris where spinal cord terminates (L1-L2)
CM lies close to nerve roots and can result in UMN and LMN features (spasticity)
May spare sacral reflexes

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29
Q

Cauda equina

A

Damage to lumbar and sacral nerve roots (L2 and below)
LMN injury
Loss and flaccid bowel and bladder
Affects more than just one nerve root
Surgical emergency
Usually bilateral leg pain/numbness, sacral root problems, urinary retention, stool incontinence, absent reflexes

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30
Q

Spastic bladder

A

Injuries ABOVE conus medullaris
Messages still travel between bladder and spinal cord
Tapping may trigger emptying
Bladder can be trained to empty on its own
Catheters or condom/foley drainage

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31
Q

Flaccid bladder

A

Injuries below conus medullaris
Messages do not travel between bladder and spinal cord
Loses ability empty reflexively
MUST be catheterized

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32
Q

Autonomic System: Sympathetic NS

A

Fight or flight response
Thoracic and lumbar portions of the spinal cord
Increase blood flow to muscles
Relaxes bronchial muscles for increase in O2

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33
Q

Autonomic System: Parasympathetic NS

A

Rest and digest
Cranial and sacral nerves
Restores energy and maintains bodily fluids
Decrease HR
Increase blood flow to smooth muscle
Contracts bronchial muscles

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34
Q

Autonomic NS dysfunction in SCI
With SNS dysfunction (T6 and above)

A
  1. Decrease HR: vagus nerve still intact from PSNS so lower heart rate… not a good way to track exercises
  2. Decrease BP: altered HR control and decreased muscle tone in LE contribute to this
  3. Poor regulation of body temperature: will go up and down with environmental temperature, messages about temperature are blocked by NLI, ensure proper hydration during session
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35
Q

Reasons for dizziness in SCI population

A

Autonomic dysreflexia, orthostatic hypotension, hypoglycemia

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36
Q

Autonomic dysreflexia

A

AT or ABOVE T6
Noxious stimuli below the NLI causes sympathetic response (blood vessels restrict)
Causes sharp rise in BP is controlled by the vagus nerve ABOVE the NLI leaving below to still be in sympathetic response
Above the NLI: sweating, flush, bradycardia
Below the NLI: chills, pale, cool, clammy, dizzy, nausea

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37
Q

Response to autonomic dysreflexia

A

If standing, sit them down
DO NOT lay flat
Try to find noxious stimuli - check bladder/catheter, bowel impairment (bladder irritation 75-85% of cases)
If above 150 BP then pharmacological management
If left untreated, can lead to hemorrhage, retinal detachment, seizures or death

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38
Q

Spinal shock
Cause
S/S
Time frame

A

Cause: acute SCI
S/S: suppression of all reflex activity below the NLI
Time: Last days - months

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39
Q

Neurogenic shockCause
S/S
Time frame

A

Cause: acute SCI, T6 and above ONLY
S/S: loss of sympathetic vascular tone and unopposed parasympathetic response… 1) bradycardia, 2) hypotension, 3) hypothermia
Time: within 30 minutes of injury and can last 6 weeks
Can be life-threatening if not treated

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40
Q

SCI Health Risks

A
  • Pressure sores/wounds
  • Poor secretion clearance
  • DVT and PE = lack of muscle pump action
  • Heterotrophic ossification (avoid forced PROM and serial casting) = treat within tolerable limits
  • Osteoporosis
  • Post traumatic Syringomyelia = formation of abnormal tubular cavity in the spinal cord
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41
Q

SCI Exercise Recommendations

A

Aerobic - 2x/week, mod - high intensity, 60-80% HR, 11-14 RPE, talk test, 20-40 mins
Strength - 2-3x/week

42
Q

LMNL
Type of paralysis
Reflex response
Response to muscle
Conduction velocity of nerve

A

Type of paralysis - flaccid
Reflex response - HYPO, no clonus
Response to muscle - atrophy present
Conduction velocity of nerve - reduced

43
Q

UMNL
Type of paralysis
Reflex response
Response to muscle
Conduction velocity of nerve

A

Type of paralysis - spasitc, hypertonia
Reflex response - HYPER, clonus
Response to muscle - delayed atrophy
Conduction velocity of nerve - unchanged

44
Q

Spasticity

A

Velocity-dependent increase in stretch reflex with tendon jerks
Hyperexcitability

45
Q

Spasticity PROS

A

Muscle bulk, help in transfers and moving limbs
Acts as a warning sign

46
Q

Spasticity CONS

A

Contractures, painful, positioning difficulties, fatigue

47
Q

Spasticity treatment

A

Medications - intrathecal baclofen, botox
Therapeutic exercise

48
Q

Assessment of Tone

A
  1. Explain purpose of interaction
  2. Ensure patient is relaxed
  3. Compare side to side
  4. Ask patient to perform AAROM
  5. Perform PROM
  6. Palpate appropriate muscles
  7. Quick stretch
  8. Reflexes
49
Q

Vestibular Disorders: Overview

A

Causes of dizziness: cardiovascular, neurological, visual, psychogenic, cervicogenic, medications, vestibular

50
Q

Functions of Vestibular System

A

Gaze stabilization - objects in visual field stay clear with head movements
Postural stabilization - maintain balance and equilibrium
Spatial awareness - understand where you are in space

51
Q

Vestibular Anatomy: Semilunar canals

A

3 canals: stimulate vestibulo-ocular reflex (VOR) and detect rotational movements
- Movement of fluid that pushes on cupula which contains hair cells
Horizontal canal: detects rotation of the head around a vertical axis (pirouette)
Anterior and posterior canal: detects rotation of the head in the sagittal plane (nodding) & rotation in frontal plane (cartwheel)

52
Q

Vestibular Anatomy: Otolith Organs

A

2 organs: detect acceleration and deceleration, sense static head position (relative to gravity)
- Movement of otoconia (crystals) causes stimulation in hair cells, and signals project to muscles that control posture
Saccule: detects vertical plane motion (elevator) & tilting head forward/backwards
Utricle: detects horizontal plane motion (acceleration in car) & tilting of head side to side

53
Q

Vestibular Ocular Reflex

A

Maintain stable vision during head movement by producing eye movements in the direction opposite to head movements
Enables to keep eyes focused/fixated on an object while we move around in space
Deficient with unilateral or bilateral vestibular loss

54
Q

Spinal Reflexes for the Vestibular System

A

Lateral and medial vestibulospinal and reticulspinal

55
Q

Vestibular Symptoms

A

Vertigo: room spinning (nystagmus), occurs with BPPV
Dizziness: being off balance, instead, having discrepancy between right and left side, don’t know where they are in space
Oscillopsia: blurred vision due to objects in vision jumping/oscillating
Nystagmus: involuntary, rapid and repeated movement of the eyes, horizontal with torsional component in peripheral vestibular issues, vertical in CNS
Hearing, light-headedness, nausea, migraines

56
Q

Vestibular Conditions: Benign Paroxysmal Positional Vertigo (BPPV)

A
  • Displacement of otoconia crystals from otolith organs
  • Otoconia displaced more often in POSTERIOR SEMILUNAR CANAL
  • Presentation: brief transient vertigo when looking up/down, rolling to that side of the bed, sitting to supine, bending forward to pick something up
  • Due to crystals creating an illusion of motion
  • Dix-Hallpike: test for vertigo, head rotated to 45 degrees and neck extended to 30, patient lowered from sitting to supine and stay for 30 seconds… positive if nystagmus is present
  • Contra to Dix-Hallpike: RA, vertebral artery insuff., 5D’s
  • Treat: Epley’s maneuver
57
Q

Vestibular Conditions: Unilateral Vestibular Loss (UVL)

A
  • Unilateral peripheral vestibular dysfunction
  • Causes: infection (vestib neuritis, labyrinthitis), disease (Meniere’s), trauma, BPPV
  • Meniere’s: disease of the inner ear due to over-accumulation of endolymph –> episodes of vertigo, unilateral nerve deafness, low frequency hearing loss, tinnitus, sense of pressure in ears
  • Acoustic neuroma: benign growth forming on the cells of CN VIII (8)
  • Presentation: dizziness (worse with movement), oscillopsia, imbalance between the left and right vestibular systems, acute nystagmus
  • Tests: head thrust test, symptoms with quick head movements (including walking)
58
Q

Vestibular Conditions: Bilateral Vestibular Loss (BVL)

A
  • Causes: toxicity, bilateral vestibular infections, vestibular neuropathy, otosclerosis (hardening of inner ear tissue), gentamicin (antibiotic that can have toxic destructive effect on the vestibular system)
  • Presentation: very poor balance, no senstation of dizziness or vertigo because there is no mismatch between the left and right side
  • Test: ++ Rhomberg, + eyes closed
59
Q

Vestibular Conditions: Central Vestibular Disorders

A
  • Causes: TIA, stroke, head injury, brain tumor, MS
  • Direction changing nystagmus, vertical nystagmus
  • Recovery dependent on cortical reorganization
60
Q

Posture: Posture Pain Syndrome

A

Pain that occurs from mechanical stress when a person maintains a faulty posture for a prolonged time period

61
Q

Postural dysfunction

A

Adaptive shortening of the soft tissues and muscle weakness that develop due to prolonged poor posture habits, positions assumed following trauma/surgery, structural faults

62
Q

Scoliosis

A
  • Named relative to convexities of the curves, with apex defining the vertebral level
  • Rotation of spine towards side of concavity causes ribs to be more prominent posteriorly on convex side, especially with flexion of spine, shoulder may also be elevated on convex side
  • 5-7 degrees or less of scoliosis is considered normal
  • 15 degrees is treatable with exercises
  • Usually involved the thoracic and lumbar regions
  • Typically right handed –> mild right thoracic and left lumbar S curve or mild left thoracolumbar c-curve
    -Structural irreversible but functionally reversible
  • Structures stretched on convex side and compressed on concave side
63
Q

Scoliosis Treatment

A

Education of importance of exercise and posture
Bracing if necessary
Stretching tight structures and strengthening weak structures
Postural exercise
Deep breathing

64
Q

Common Postural Imbalances: Forward head

A

Forward head postures - flexed CT junction + extended upper c-spine
Short: cervical extensors, UFT, lev scap, SCM and scalenes
Long: DNF

65
Q

Common Postural Imbalances: Lumbar Lordosis

A

Pelvis positioned forward and downward (anterior tilt)
Hips are slightly flexed, lumbar spine hyperextended
Short: erector spinae, hip flexors
Long: Abdominals, hamstrings and glute max

66
Q

Common Postural Imbalances: Posterior Pelvic Tilt

A

Flat back, posterior pelvic tilt
Short: tight abdominals. hip extensors (hamstrings and glute max)
Long: hip flexors, erector spinae

67
Q

Common Postural Imbalances: Thoracic Kyphosis

A

Often associated with scapular and cervical postural deviations
Short: pec minor and major
Long: PLL, erector spinae and scap retractors
May cause TOS

68
Q

Common Postural Imbalances: Genu recurvatum

A

Knee hyperextension
Causes: shortened gastrocs, severe spasticity of quads, weakness of quads, anterior pelvic tilt

69
Q

Balance Strategies: Ankle

A

1st Strategy
Maintain balance for small amounts of sway
Dorsiflex and plantar flex

70
Q

Balance Strategies: Hip

A

2nd Strategy
Larger faster displacements
Quads, abdominals, erectors, hip extension

71
Q

Balance Strategies: Step

A

3rd Strategy
Perturbation are fast or large amplitude OR when other strategies fail
Last strategy before fall

72
Q

Balance Testing: Sitting Progression

A
  • Base of Support: Feet wide - narrow BOS - feet together
  • Internal perturbations: reach within BOS, outside BOS, turn and look over shoulder
73
Q

Balance Testing Sitting: Expected External Perturbation

A
  • Inform patient on which way to push
  • Push patient back, side to side and forward
74
Q

Balance Testing Sitting: Unexpected external perturbation

A
  • do not tell which way going to push
  • stand in front of patient and gentle push
75
Q

Balance Testing Standing: BOS

A
  • SLS, tandem
76
Q

Balance Testing Standing: Internal Perturbations

A
  • Reaching within base of support - reach outside os BOS
77
Q

Balance Testing Standing: Expected External Perturbations

A
  • Inform patient on which way to push
  • Push patient back, side to side and forward
78
Q

Balance Testing Standing: Unexpected external perturbations

A
  • do not tell which way going to push
  • stand in front of patient and gentle push=
79
Q

TBI: Mechanisms - Primary

A

Primary Brain Injury: damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed or torn
- Can be local and/or diffuse
- Coup: damage at the site of impact
- Contracoup: damage may occur on the side opposite the impact if the force is great enough to cause the brain to move in the opposite direction
- Diffuse axonal injury from rotational and/or deceleration forces (stretch and tear the nerve)
- Penetrating brain injury
- Focal injury: contusion, laceration, hematoma

80
Q

TBI: Mechanisms - Secondary

A

Secondary: brain damage that is an indirect result of the initial injury
- Occurs immediately to days after injury
- Ongoing damage from: ischemia, cerebral edema (ICP), release of free radicals, electrolyte imbalances, excessive release of glutamate (neurotoxic at high levels)

81
Q

TBI: Intracranial Pressure

A

Normal is 0-15mm Hg > 20 mm HGg BAD
Head down position is contra indicated
Head of bed should be elevated to 30 degrees

82
Q

TBI: Cerebrospinal Fluid (CSF)

A
  • Produced in choroid plexus in the ventricles
  • Nourishes and cushions the brain
  • CSF is constantly being produced (500mL daily)
  • CSF constantly being reabsorbed (150mL daily)
  • Excessive production, diminished absorption or a blockage in the ventricular system can head to HYDROCEPHALUS and elevated ICP
83
Q

TBI: Basal Skull Fracture

A
  • Rare
  • Can cause a tear in the meninges resulting in CSF leakage
  • Signs are blood or CSF in nose/ears, racoon eyes, bruising over mastoid (battle sign)
  • NEVER DO NASAL SUCHIONING OR PUT NG TUBE
84
Q

Coma

A

State of unconsiousness in which thre is neither arousal nor awareness - no amount of stimulus (or only pain) will cause patient to respond

85
Q

Glasgow Coma Scale

A

Eye opening, verbal response, motor response
Scored from 3-15
Mild brain injury 13-15
Moderate brain injury 9-12
Severe brain injury 8 or less

86
Q

Ranchos Los Amigos Level of Cognitive Functioning

A
  • Does not predict over long term
  • Evaluation tool that helps understand behaviour and progression of brain injury over time
  • Useful for therapists when helping design an appropriate treatment program
  • 1 = no response, 5 = confused, 10 = normal
87
Q

Treatment for Patients in Coma

A
  • Suctioning: pre/post O2 to 100%
  • Chest physio
  • Positioning: limit neck flexion and rotation
  • PROM
  • Resting splints 6-8 hrs to prevent contractures
  • Mobilization: dangle, lift to chair
  • Aspiration risk: turn feed tube OFF 20 minutes prior to treatment
88
Q

TBI: Initial Management

A
  • Prevent hypoxia, maintain adequate BP, adequate fluids to maintain mean arterial pressure, HOB 30
  • Nutrition: hypermetabolism
  • Increase in muscle tone and issues with temperature regulation
    (Brian glucose metabolism rate is increased after TBI due to the metabolic cascade of events)
89
Q

TBI: Decoricate Positioning

A
  • LE is extended and IR with feet in PF
  • UE is in shoulder adduction, elbow flexion and wrist/finger flexion
  • Indicates damage ABOVE RED NUCLEUS
  • Damage in midbrain of brain stem
90
Q

TBI: Decerebrate Positioning

A
  • Neck extended
  • LE is extended and ER with feet in PF
  • UE is in extension, internal rotation with elbow extension and wrist flexion
  • Indicated damage AT OR BELOW RED NUCLEUS
  • Damage to the brain stem or cerebellum
91
Q

TBI: Hemorrhage & Hematoma

A
  • Hemorrhage: bleed
  • Hematoma: collection of clotting blood
  • Damage can be from anoxia or pressure
  • Intracranial hemorrhage: bleeding within the skull –> can increase ICP
92
Q

TBI: Subarachnoid Hemorrhage
- Location
- Vessels involved
- Symptoms (depending on severity)
- Treatment

A
  • Location: very high pressure arterial bleed between arachnoid and pia mater
  • Vessels involved: arteries –> circle of Willis
  • Symptoms (depending on severity): rapid onset of severe headache, vomiting, confusion, decreased level of consciousness, possible CN 3 warning with dilated pupils
  • Treatment: requires surgical intervention to stop bleed
93
Q

TBI: Sub-dural Hematoma
- Location
- Vessels involved
- Symptoms (depending on severity)
- Treatment

A
  • Location: low pressure venous bleed with blood collecting between dura and arachnoid mater
  • Vessels involved: veins
  • Symptoms (depending on severity): onset occurs over hours, fluctuating symptoms, appears drunk
  • Treatment: often requires surgery (burr holes or craniotomy)
94
Q

TBI: Epidural Hematoma
- Location
- Vessels involved
- Symptoms (depending on severity)
- Treatment

A
  • Location: rapid arterial bleed occuring between cranial vault and dura, 90% associated with skull fractures, most often in temporal or tempopartieral region (thin bone)
  • Vessels involved: arteries (middle meningeal artery)
  • Symptoms (depending on severity): “talk and die”, initial feels normal then declines to LOC
  • Treatment: medical emergency ensure ABCs, transport immediately
95
Q

Cerebellar Disorders: Pathophysiology

A

Cerebellum modifies muscle activity so dysfunction affects QUALITY of movement (precision, timing, accuracy of motor output)
Damage can come from tumor, stroke, infection, trauma, chronic alcoholism

96
Q

Cerebellar Disorders: Presentation

A

Degeneration will typically present with dysmetria, nystagmus, dysdiadochokinesia
IPSILATERAL signs and symptoms
Effects vestibular equilibrium, posture and synergy of movement, fine coordination
- May present with: loss of balance, coordination deficits, functional disabilities (intention tremor), motor learning impairments, cognitive deficits, emotional dysregulation, minimal strength deficit, may have fatigue issues, hypotonia, hyporeflexia due to lack on intensity of input

97
Q

Cerebellar Disorders: Therapy Goals

A

Improve coordination, improve postural stability and balance, improve functional mobility, improve vestibular functioning, cardiovascular endurance

98
Q

Cerebellar Disorder: Examples

A

MS, Hereditary ataxia (degeneration), Friedreich’s ataxia (gene defect)

99
Q

Non-cerebellar coordination issues: Examples

A

Athetosis - slow continuous involuntary movements
Chorea - rapid jerky coarse movements
Dystonia - twisting and repetitive movements causing abnormal postures caused by simultaneous contractions of opposing muscle groups
Hemiballsmus - sudden stabbing movements of one side of the body

100
Q

Balance Issues Testing: Rhomberg

A

Stand in corner
Testing 3 systems responsible for balance - vestibular, proprioception & vision

101
Q

Coordination Testing

A

Dysdiadochokinesia testing - UE = rapid alternating movements of pronation and supination, LE = rapid alternating toe tapping

Dysmetria testing - UE = fingertip to thumb, finger to nose, opposition, LE = heel slide on shin

Physio (11 decks)

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