Week 19-20 - Peripheral Neuropathy & Spinal Cord Injury Flashcards
1
Q
Epineurium
A
Surrounds entire nerve
2
Q
Perineurium
A
Encapsulates fascicle of nerves (bundles of axons)
3
Q
Endoneurium
A
Contained within the perineurium and coating axons.
4
Q
Blood-nerve barrier
A
between inner perineurium and endothelial cells of microvasculature within endoneurium
5
Q
What are special senses?
A
Modalities that are carried by cranial nerves (i.e., olfaction, vision, tase, hearing/balance)
6
Q
What are somatic senses?
A
Detected from all parts of the body (and head) and transmitted to the CNS via all spinal nerves except for C1 and the trigeminal nerve. Distinct from special senses, which are only carried by cranial nerves (i.e., vision, taste)>
7
Q
Types of sensory receptors (4)
A
photoreceptors (rods and cones) thermoreceptors (central and peripheral) Nociceptors Mechanoreceptors (exteroreceptors and proprioceptors)
8
Q
2 types of mechanoreceptors
A
Exteroreceptors respond to stimuli from outside the body (i.e., touch);
Proprioreceptors give information about position of the body, or its parts.
9
Q
Generator potential vs action potential
A
Generator Potential is graded in amplitude (bigger stimulus has bigger GP) and does not cause the membrane to be refractory, nor does it actively propagate. Action potentials are all or nothing. They do cause membrane to bcm refractory to prevent backward propagation and they are actively propagated by regenerating themselves along the axonal membrane.
10
Q
what is meant by the concept that the neuromuscular junction has a high safety factor
A
This refers to the fact that every alpha motor neuron AP will result in a muscle AP and subsequent contraction. Many parts of the physiology have developed to make this the reality (lots of VGNaCs etc).
11
Q
Definition of anemia
A
A decrease in blood hemoglobin concentration. Can be the result of decreased RBCs or increased plasma. Normal ranges are age and sex dependent so the diagnosis of anemia differs based on these characteristics.
12
Q
best marker for iron deficiency
A
Ferritin. Ferritin < 30 indicative or iron deficiency.
13
Q
most common cause of iron deficiency anemia in the developed world is… What are the other causes of iron deficient anemia? (3)
A
Most common is occult blood loss! Bleeding Diet deficiency Malabsorption Increased need (children, pregnant)
14
Q
What are the causes of microcytic anemias?
A
Acronym: TAILS Thalassemia trait Anemia of chronic disease Iron deficiency Lead poisoning Sideroblastic anemia
15
Q
How are the generator potentials produced by mechanoreceptors, nociceptors, chemoreceptors, and photoreceptors different?
A
Mechanoreceptors produce a generator potential DIRECTLY in response to stretch (Na/K channels open in response to stretch). In contrast, nociceptors, photoreceptors, and chemoreceptors produce generator potentials INDIRECTLY via GPCRs.
16
Q
The neuromuscular junction includes…
A
The presynaptic terminal of the alpha motor neuron, the synaptic cleft, and the post synaptic membrane of a muscle cell.
17
Q
What is a motor unit?
A
1 alpha motor neuron and all of the muscle fibres that it innervates.
All of the muscle fibres innervated by a motor unit are the same type of fibres (fast, slow, twitch).
18
Q
What is a motor unit pool?
A
All of the motor units that are involved in the innervation of a skeletal muscle.
19
Q
Describe the basal lamina of peripheral nerves
A
it surrounds both the individual axon and myelin
20
Q
Explain action potential propagation along a motor neuron (4)
A
An AP travels along an alpha motor neuron (MN) to all of its terminal branches.
- Ca2+ influx through voltage gated Ca channels stimulates release of ACh from vesicles at the distal end of the alpha MN
- ACh binds AChRs on shoulders of post junctional folds
- Na+ and K+ flow though AChR pore, which results in muscle membrane depolarisation
- this depolarisation is the ENDPLATE POTENTIAL
- AChE in the basal lamina hydrolyzes ACh to terminate NM transmission
21
Q
Where is AChE located and its role
A
In the basal lamina/EC matrix of the synaptic cleft. Cleans up ACh swiftly so that contraction is v discrete.
22
Q
What is the point of junctional folds on the post syanptic membrane
A
Large SA for AChR activation (located on the shoulders of folds)
23
Q
What is the perijunctional zone
A
It is on the periphery of the site of muscle AP initiation. Has a high density of VGNaCs to ensure that muscle membrane reaches AP threshold (EPP is almost always large enough)
24
Q
What is the point of T tubules on muscle cells?
A
They help bring AP deep into the cell.
They are continuous with the membrane. VGCa Channels on the t tubules pair with Ryanodine receptors on the SR to induce Ca release into the muscle cell.
25
Myelin
Coating derived from Schwann cells in the PNS that is present on fast-conducting fibers, both motor and sensory promoting faster conduction.
26
Positive symptoms of peripheral neuropathy. What are they generally and the two categories.
Positive symptoms reflect inappropriate spontaneous nerve activity. May be more prominent early on. - MOTOR (cramps; twitch) - SENSORY (tingling/prickling, burning, stabbing pain, allodynia, hyperalgesia)
27
Allodynia
Discomfort to stimuli that are not typically painful (i.e., sensitive to bedsheets on toes)
28
Negative symptoms of peripheral neuropathy
Negative symptoms reflect reduced nerve activity. MOTOR - weakness; atrophy SENSORY - reduced sensation/numbness; - gait ataxia (balance is worse without visual input)
29
Autonomic symptoms of peripheral neuropathy (4 categories)
- Cardiac (orthostatic dizziness, labile BP, arrhythmias) - GI (early satiety, bloating, constipation, diarrhea) - Genitourinary (ED, urinary incontinence) - Vasomotor (cold extremities; skin colour changes)
30
Clues that it may be a demyelinating neuropathy (rather than axonal)
- weakness without atriphy - not length-dependent - early loss of reflexes - rapidly ascending sx - preceding infection
31
Why is it important to identify if a neuropathy is demyelinating type
Primary demyelination often involves an immune-mediated neuropathy, which are often amenable to treatment.
32
Causes of length-dependent, axonal polyneuropathy
Systemic metabolic disorder (i.e., diabetes, nutritional deficiencies [i.e., pernicious anemia - can't absorb B12]); Toxins (chemo, chronic EtOH); Hereditary (Charcot-Marie-Tooth); Idiopathic (elderly);
33
Principles for managing peripheral neuropathy (6)
1. treatunderlying cause (i.e., glycemic control) 2. Neuropathic Pain (pharma and non-pharma) 3. Bracing and orthotics 4. Multidisciplinary team (OT, PT, podiatry for foot care) 5. Education and counselling 6. Avoidance of neurotoxins
34
Pharmacological Management of Neuropathic Pain
1. Gabapentin, TCA, SNRIs 2. tramadol, opioids 3. cannabinoids 4. 4th line agents
35
Non-pharma management of neuropathic pain
- CBT - address depression and anxiety - Physio - OT - Aquatherapy
36
What is polyradiculopathy
Pattern in which there is evidence of involvement at multiple nerve roots and additional involvement of more distal sites of the peripheral nervous system.
37
Charcot-Marie-Tooth What is it, what causes it, and what are the features?
The most common type of hereditary neuropathy. Encompasses a number of genetically distinct disorders. There are axonal and demyelinating subtypes. Insidious, symmetric progression. Usually painless with minimal positive symptoms. Often severe distal wekaness and sensory loss with little disability. Foot deformity (high arched feet and hammer toes). Usually positive family histories.
38
Guillan-Barre Syndrome
AKA Acute inflammatory demyelinating polyradiculopathy. Most common cause of acute generalized weakness. Can occur at any age. Most have had a recent infection. Sensory symptoms in periphery and trunk. Large fibre \> small fibre impairment. Distal\>proximal motor weakness - the predominant feature. Begins in legs and ascends to arms, trunk, head, neck. Can develop resp failure. Can have autonomic sx of hypo/hypertension and cardiac arrhythmia.
39
Clinical course of guillan-barre syndrom
TIMING IS SUPER IMPORTANT! progresses over 2-4 wks - plateaus - recovery over months. If they haven't reach max abnormality at 8 wks then it isn't GBS!
40
Schwaan Cells - types and functions
Can either be myelinating or demyelinating. - Produce neurotrophic & neurotopic substances - Induce receptor formation when needed - Produce extra-cellular matrix
41
3 levels of demyelination of peripheral nerve axons effect of each of these scenarios
1. Reduction in myelin thickness - slower AP propagation 2. Complete demyelination of a segment - slower AP and Na+ channel redistribution from node of ranvier 3. Complete demyelination of several adjacent segments - AP failure because Na+ channels aren't dense enough to support propagation. Loss of nerve cell function as long as the AP block persists.
42
How does remyelination work?
Damaged Schwaan cells release trophic factors and cytokines. Macrophages come and clean up remaining myelin; The same factors also trigger proliferation of undifferentiated Schwann cells, some of which differentiate into myelinating cells and wrap around the bare axon.
43
Tinel's sign
Occurs when an axon has been disrupted/cut. If you tap on the proximal edge (connected to the brain), it will elicit pins and needs. Can be used clinically to monitor progression of axon regeneration.
44
Wallerian Degeneration
The severed chink of axon (not attached to cell body) will degenerate and won't come back. You can't re-connect two ends again and save it.
45
Peripheral nerve regeneration after injury
Cell body sends signals to upregulate factors that promote growth. Up to 10 sprouts are produced at the cut site. Each sprout has a growth cone with mobile filopodia. Interaction ebtween the growth cone and its env is key for continued elongation and direction of growth. The basal lamina from the degraded axon stump remains = the ENDONEURIAL TUBE. Schwaan cells differentiation and form pathways with the endoneurial tube to guide regrowing axon.
46
How quickly can nerves grow back?
~1-4 mm/day (and can be tracked by Tinel sign)
47
Do you get back full function after a nerve regrows?
Nope. Some sensory and motor fibres will mix up and get pruned away. Mostly sensory reinnervated sensory and vice versa so you get good recovery but not perfect.
48
What are nerve conduction studies for?
Nerve conduction studies are used to assess if it is a neuropraxia (AP block due to demyelination) or if the axons have been completely disrupted. The symptoms of these two are the same --\> loss of fxn.
49
Results of nerve conduction study with neurapraxia
The axon is intact, but demyelination stops AP from continuing to the end. If the stimulator and receiver are placed on one side of the gap then it will transmit, but if they are on opposite sides of the gap then the signal won't transmit.
50
Results of a nerve conduction study in the case of severed axon
Initially (before) wallerian degeneration), the study will look a lot like neurapraxia because the severed stump still exists and transmits a signal. Just like in neurapraxia, the signal won't bypass the gap if signal and receiver are placed on either side of it. After 2-3 weeks, the stump has degraded and you won't get any conduction on the distal end because there is nothing there. Decreased velocity of transmission for a demyelinating disorder.
51
Neuroma
A lump of nervous and connective tissue that may develop after a severed nerve heals.
52
Neuropathic pain vs nociceptive pain
Nociceptive pain occurs with tissue damage or potentially-damaging stimuli. Neuropathic pain is chronic pain that results from lesions in or dysfunctions of the nervous system.
53
Lidocaine
An aminoamide local anaesthetic with reasonable safety profile. Fast onset and intermediate duration of action. Used IV as an antiarrhythmic and in acute and chronic pain (also subcutaneous).
54
Lidocaine
An aminoamide local anaesthetic with reasonable safety profile. Fast onset and intermediate duration of action. Used IV as an antiarrhythmic and in acute and chronic pain (also subcutaneous).
55
Monosynaptic stretch reflex
* 1a fibres from muscle spindles sense the quick stretch of muscle
* 1a fibres synapses with interneuron in the spinal cord
* Interneuron coordinates
* _contraction of the agonist muscle_ (knee goes up) _and the antagonist muscle_ (relax knee flexor)
56
Spinal reflex
A reflex to maintain muscle tone. This is different from a monosynaptic reflex! It is mediated by continuous excitation of gamma motor neurons. This reflex is initiated centrally, which is why an upper motor neuron lesion will cause increased tone.
57
What neuropathic outcomes can occur with diabetes?
There may be 4 presentations: 1) mononeuropathy (named nerve) 2) Radiculoplexopathy (plexus or nerve root) 3) Distal-symmetric (classic) 4) Autonomic neuropathy
58
Describe the pathway taken by the Corticospinal tract
2 branches: lateral and anterior corticospinal tracts
* All upper motor neurons original in the primary motor cortex and travel down the **internal capsule**
* Pass through **crus cerebri**
* **Lateral corticospinal tract** accounts for 85% of fibres and is responsible for controlling limb muscles
* _Decussate_ at **medullary pyramids**
* _Synapse_ at traget spinal level with the lower motor neuron
* LMN exits ventral horns
* **Anterior corticospinal tract** accounts for 15% of fibres and is responsible for controlling muscles of the trunk
* Does not decussate in the medulla. Descends down spine.
* _Decussates_ at target spinal level and _synapses_ with LMN in the ventral horn.
59
Describe the path taken by the Dorsal Column-Medial Lemniscus Pathway
DCML Pathway carries modalities of touch, proprioception, and vibration. It includes groups I and II (myelinated and fast) fibres.
* Cell body located in the **dorsal root ganglion**
* Fibres from *below T6* ascend the spinal cord in the **gracilis fascicle**
* Fibres from *above T6* ascend the spinal cord in the **cuneate fascicle**
* Fibres _synapse_ with 2nd order neurons in the **gracilis/cuneate nuclei** in the medulla and then _decussate_ to rise in the **medial lemniscus**
* Fibres _synapse_ with 3rd order neurons in the **ventroposterior lateral (VPL) nuclei of the thalamus** (home of sensory fibres from neck down)
* 3rd order fibres ascend to the sensory cortex where they _synapse_ on final 4th order neurons.
60
Describe the path taken by the Spinothalamic Tract
The spinothalamic tract carries pain, temperature, pressure, and crude touch sensation.
* The primary neuron cell body is in the **dorsal root ganglion.**
* It _decussates_ within a few spinal levels of entering the spinal cord and _synapses_ on a second order neuron
* Second order neuron splits into the **lateral tract** (which carries pain, pressure, and temperature) and the **anterior tract** (crude touch).
* The tracts rise up and _synapse_ with a 3rd order neuron in the VPL of the thalamus, which then goes up to synapse with a 4th order neuron in the primary somatosensory cortex.
61
What are some additional exams that you would do for a spinal cord injury patient (in addition to myotome and dermatome testing).
DRE
Bulbocavernosus and cremasteric reflex
62
Bulbocavernosus reflex: How does it work? What is it controlled by? What does its presence/absence suggest?
Squeeze glans clitoris or penis and the bulbocavernosus muscle should contract. This is mediated by the pudendal nerve (S2-4) - a spinal reflex. If absent, suggests a LMN lesion. If present, suggests UMN lesion.
63
Spinal Shock
Transient state immediately after spinal cord injury.
May include loss of reflexes and autonomic dysregulation. In fact, dysregulated high BP can cause stroke at this time. This is why we have to reassess these pts frequently, becaue their spinal shock may mask function that was preserved in the injury.
0-24 hr post-injury - areflexia below level of injury
1-3 days post-injury - return of reflexes (especially cutaneous reflexes)
4 days - 1 mo - hyperreflexia development would suggest an UMN lesion
1-12 mo - spasticity, clonus, hyperreflexia
64
What is the cremasteric reflex responsible for?
Thermoregulation of the scrotum
65
5 stages of grief
Denial, anger, bargaining, depression, acceptance
66
Autonomic Dysreflexia
* MEDICAL EMERGENCY
* A syndrome of excessively high BP in response to noxious stimulus (SBP \> 20 mmHg from baseline)
* Common in people with spinal cord injury, **especially in T6 or higher**.
* Any noxious stimulus (i.e., full bladder) below the level of injury is not sensed cognitively, but the body reacts in an intense way.
* Can lead to seizure, stroke, or even death if not addressed/treated promptly. Symptoms may include headache, axious feeling, flushing/sweating, nasal stuffiness, bradycardia, goose bumps, cold/clammy below level of injury.
67
Neurogenic bladder: What are the **two kinds**, at **what levels** do they occur?
**Spastic (reflex) bladder**: Lesion at or above **TXII** (**spinal level S2**)
* involuntary bladder contractions
* bladder ocntraction and sphincter relaxation are generally uncoordinated
* Results in urine leakage and difficulty voiding when spasms occur
**Flacid (atonic/overflow) bladder**: Lesion below TXII (spinal level S2)
* Large, dilated bladder - results in bladder dapage due to overstretching
* Loss of sphincter coordination and detrusor muscle contration --\> makes it hard to initiate voiding
* Symptoms: overflow incontinence
68
Describe the anatomy of the bladder and sphincters (briefly)
Detrusor muscle is the main muscle. Males have an internal sphhincter and a prostate. Both males and females have an external sphincter.
69
Describe neurologic control of micturition: Upper centres (3) and local input (4)
The frontal cortex controls micturition consciously. The **pontine micturition centre** receives parasympathetic input from stretch receptors to tell us when bladder is full. The **periaquaductal grey** coordinates input from cortex (socially acceptable time to pee) and sensory (when you know you gotta go).
The **hypogastric nerve (sympathetic**) arises from T12 to L2. It relaxes the detrusor muscle and contracts the internal sphincter (in males). So it is active during during filling and inactive during voiding.
**Parasympathetic input** comes from S2,3,4. It contracts the detrusor muscle so it is active during voiding and inactive during filling.
The **pudendal nerve** is under somatic control. It comes from S2, 3, 4. It is tonically active and contracts the external sphincter. It is therefore active during filling and consciously relaxed during voiding.
The **pelvic nerve (*pee time nerve)*** fires slowly when the bladder is relaxed, relaying positive input to the hypogastric nerve (relaxes detrusor and contracts internal sphincter). The pelvic nerve fires quickly when the detrusor muscle is stretched, causing it to ascend to pontine micturition centre and tell us we gotta go!
70
What are some tests for sexual potential (5)
1. _Bulbocavernosis reflex -_ +ve suggests reflex arousal with stimulation but -ve _doesn't mean much because this reflex is absent in 15-30% healthy people_
2. _Hip reflex_ - +ve suggests reflex arousal with stimulation but -ve doesn't mean much because this reflex is absent in 15-30% healthy people
3. _Pinprick sensation_ - +ve suggests orgasm possible
4. _Voluntary anal contraction_ - +ve suggestz orgasm possible
5. _anal tone_ - +ve supports intact lumbosacral autonomics (better chance of ejaculation)
71
What are the effects of spinal cord injury on fertility?
Women can get pregnant but there will be issues during pregnancy and in delivery.
72
The role of muscle spindle
Muscle spindles are fibres in the muscle cell that act as mechanoreceptors. They communicate with CNS via **1a afferents** where there is a *change in in length (i.e., fire during dynamic stretch)*, so we can maintain posture.
73
Gamma vs alpha motor neurons
Gamma - "Gain"
* Intrafusal fibres that adjust spindle tension from the inside [Intrafusal = inside the bundle of muscle fibres (actin and myosin)]. They tune muscle responsiveness to input in order to optimize our ability to generate force at different lengths.
* Important for postural reflexes and proprioceptive reflexes
Alpha - "Action"
* Extrafusal fibres that contract muscle. They get input from corticospinal tract (and others).
These are both ventral horn exiting and heavily myelinated
74
Rubrospinal tract
- Arises in red nucleus
- involved in maintaining flexor tone in the arms (limited to cervical spinal cord)
75
Reticulospinal Tract
- Brainstem reticular activating system
- involved in postural control and tone
- Primary regulates extensor tone, more axial muscles
76
Gamma/Alpha Coactivation
An intended movement will result in both gamma and alpha motor neuron activation. This keeps the muscle spindles taut as muscle contracts so the muscle can remain sensitive to touch.
77
Proprioceptive reflexes
Coordinate activity of agonist and antagonist muscle pairs. This is critical for maintaining posture.
78
Brown Seqard Syndrome. Give an example of what would occur.
Lesion to 1/2 of spinal cord. The pure syndrome is rarely seen (maybe a gunshot wound through hald of the SC), but common on exams ;)
Results (if it was L spinal cord):
* lost vibration, position, and deep touch sensation from the L side of the body
* Lost pain, temperature, light touch on right side
* Paralysis below this level on the L side of the body
79
How do we quantify the extent of a spinal cord injury?
Using the ISNCSCI (aka ASIA exam) Exam = International Standards for Neurological Classification of Spinal Cord Injury.
This involves going through each dermatome and myotome to check for preserved sensation/motor capacity. Physical exam findings include: sensation (light touch, pin prick), motor strength, and digital rectal exam.
80
Grading scale for sensation
0 - absent
1 - present but not normal
2 - normal
81
Grading scale for motor power
0 - no contraction
1 - flicker or less than full range without gravity
2 - full range without gravity
3 - full range against gravity
4 - full range against some resistance
5 - normal power
82
How is a complete SCI different from an incomplete SCI?
An incomplete SCI has some sensory or motor function preserved in the sacral segments (S4-5). This is why the digital rectal exam is so important!
83
What is the prognosis after spinal cord injury? Will function improve?
* Best based off of exam 3-7 days after the injury (b/c spinal shock)
* 50-90% chance recovery in nearby myotomes
* Most SCIs that are complete remain complete
* Most recovery is achieved in the first few months, but may continue to improve over the next 2 years.
84
What are the important levels of spinal cord injury for v different prognoses?
C1-3: likely ventilator-dependent
C7: most common level for functional independence
T6 and above: at risk for autonomic dysreflexia
Lumbar level and below: mostly LMN injury
85
What is the ASIA Impairment Scale?
Clssifies completeness of the spinal cord injury.
A - complete
B, C, D - incomplete
E - no neurologic deficit
86
87
Central Cord Syndrome
Most common incomplete spinal cord injury syndrome
* Upper extremities more involved because of somatotopic organization (they are closer to the centre of the cord!)
* Possible bowel/bladder involvement
88
What are 2 risk factors for central cord syndrome?
Hyper-extension injury
Narrowing of the cervical spine (cervical stenosis; common in older population)
89
Anterior Cord Syndrom
* Worst prognosis of the incomplete soinal cord injury syndromes
* The area supplied by the anterior spinal artery is affected (spinothalamic and cerebrospinal)
* Presents with motor deficit, pain/temp deficit; often bladd dysfunction; proprioception/light tough relatively preserved
* Poor motor return
90
28 year old experienced significant low back
pain when lifting boxes two days earlier. This
morning he has numbness and weakness in
his legs. He had a slow stream of urine. He has
come to your office to treat the pain.
This is **Cauda Equina Syndrome!** It is a surgical emergency.
* A LMN injury
* **low back pain is common** so always scan for this in the pt w low back pain
* Various presentation:
* Sudden onset of pain/neurological symptoms in a pt with no previous lower back pain.
* Acute onset of neurological symptoms with history of lower back pain and sciatica
* Gradual progression of neurological symptoms in patient with history of lower back pain and sciatica
* Key Sx: saddle anasthesia, new urinary dysfxn, new sexual dysfxn, pain/weakness in legs, loss of ankle reflex.
* 85% cases signs and sx develop in less than 24h
* Prognosis: depends on degree of injury and time until treatment. It's a LMN lesion so potential for nerve regrowth.
* Bowel and bladder and sexual dysfxn can be prolonged
91
How would sexual arousal look with a cervical spinal cord injury?
Reliant on reflexogenic pathway to induce sexual arousal. This means that touch to genitals will likely still elicit vasocongestion (erection).
92
How would sexual arousal in the case of a sacral injury?
A sacral injury may interfere with the reflexogenic pathways (S2-S4) so genital arousal would mostly be dependent on mental arousal. Touch to genitial would not elicit vasocongestion.
93
Ejaculatory Inevitability
This is the "point of no return" between the two phases of male ejaculation (seminal emission --\> propulsatile ejaculation)
Closure of the bladder neck with seminal emission with concomitant closure of the external sphincter increasing intraprostatic pressure.
94
Explain male ejaculation: Branches of the nervous system involved, their spinal levels, the nerves, and the roles of each part
95
How are vasocongestion and orgasm impacted in radical pelvic surgeries?
Typically compromise vasocongestion but spare orgasm in both men and women
96
How does vasocongestion in erection work?
Neural signals release NO at the genitals. NO works via cGMP, which tells smooth muscle to relax so blood can flood corpora cavernosa. At the same time, venules are compressed against the tunica albuginea, preventing backflow so blood is held locally.
97
How does an erection drug like viagra work?
Viagra inhibits PDE5. PDE5 inhibits cGMP, which is a 2nd messenger from NO that is central in inducing muscle relaxation and htus engorgement. If we inhibit PDE5, nothing is stopping cGMP from making erections. But you must have some mental arousal going on in the first place to make this work, otherwise, there won't be any NO and cGMP around in the first place.
Usually PDE% inhibitors do not work for female sexual dysfunction unless it is a neurological issue. Usually erectile tissu eis already maximally engorged and it is a mental arousal issue
98
How can we bypass the need for mental sexual arousal to get genital arousal?
Mental arousal is reponsible for the NO that eliits erection. If we can't get the mental arousal down there, we can inject PGE (direct vasodilator) or use vacuum devices.
99
When may penile vibro stimulation be helpful?
When there is an intact lumbosacral cord. More likely to work if pt has reflex erection and intact bulbocavernosus reflex.
100
When may electroejaculation be helpful?
When there is a SCI below T10, thus damaging the lumbar-sacral cord. This is a rectal probe that can jump start the efferent pathways of seminal emission. Use for making babies. May require general anaesthesia.
101
Orgasm after spinal cord injury
* up to 50% of women and 40% of men are able to achieve a sense of release or altered orgasm (with or without ejaculation)
* Vibrators help
* Orgasmic sensations can either be genitally derived or may be generated from other sensate areas that elicit brain arousal or from fantasy.
102
Hyperreflexive Bladder
Neurogenic bladder associated with UMN lesion
* Reduced ability to sense full bladder
* Overactivity of detrusor and (external sphincter) - involuntary baldder contractions
* Loss of coordination bt detrusor and sphincter (because the pontine micturition centre no longer has a connection to the bladder)
* Results in
* urine leakage
* difficulty voiding when spasms occur
* **Detrusor external sphincter dyssynergia**: Bladder is full but that message doesn't get to the brain to relaz sphincter. Urine may back up and bladder may hypertrophy due to pressure. CAUTION RE: RENAL HEALTH
103
Treating hyperreflexic bladder
Catheterization (intermittent or indwelling)
104
Complications of neurogenic bladder
* Commonly: **UTIs,** **blocked catheter, incontinence**
* Long term: renal dysfunction (from urine backup), detrusor hypertrophy, increased risk of cancer (especially if indwelling foley catheter).
105
Neurogenic bowel presentation
In spinal cord injury, neurogenic bowel typically results in...
* Prolonged bowel transit time
* Altered sphincter control
* Constipation
* Incontinence (includin goverflow incontinence)
106
Management for neurogenic bowel
Consistent bowel management
* Diet, fluid intake
* Scheduled bowel days (to clear), medications
* UMN lesion bowel dysfunction usually required digital rectal stimulation
* Do not be fooled by overflow incontinence (looks like diarrhea, but it's overflow around huge backup!)
107
How do pressure ulcers occur in SCI?
_Extrinsic factors_: Pressure on a bony prominence, shear due to trasfer methods, friction due to spasticity, moisture fron incontinence.
_Intrinsic factors_: General health, nutrition, smoker, atrophy (bony body)
108
Preventing pressure ulcers
BE VIGILANT W SCI PTs!! Daily checks, night turns, proper equipment. These can develop within hours.
109
How does spasticity occur in SCI?
UMN lesion causes hyperexcitability of the stretch reflexes - Increased tonic stretch reflexes with exaggerated tendon jerks.
110
Upper motor neuron syndrome
_Positive signs:_ Spacticity, rigidity, hyperreflexia, primitive reflexes, clonus
_Negative signs_: Lack of strength, control coordination
111
Approach to spasticity
- Describe the spasticity (focal or global, rate, complications and benefits)
- Identify underlying cause
- Decide if it needs to be treated at all.
- Treatment:
* Stretching and positioning
* Medication - **Baclofen** (commonly causes drowsiness); marijuana (with more research), injections (**botulinism toxin**), surgery (intrathecal baclofen pump)
112
Blood pressure changes with SCI
* Resting BP is typically lower than prior to injury (especially in tetraplegia) - 90-110
* **Orthostatic hypotension** = episodes of low BP upon change in body position from supin to upright. Pt may feel light-headed, dizzy, fait, blurry vision, fatigue
113
How to manage orthostatic hypotension
Tends to improve with time.
* Sit up slowly
* Lower head (i.e., tilt chair) if symptomatic
* Ensure proper hydration
* COmpression stockings and abdominal binder (not always tolerated well longterm)
* Medications if symptomatic
114
Stimuli that may bring on autonomic dysreflexia
_Bladder_ (very common): UTI, retention, blocked catheter, kidney stone
_Bowel_
_Skin_
115
Treating autonomic dysreflexia
* Be ready to suspect it (especially with SCI above T6)
* Check BP regularly
* Try to correct the issue: Sit up (reduce cranial blood flow), loosen tight clothing, check bladder fxn
* If BP remains high, consider pharm treatment
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autonomic dysreflexia is more likely if...
Spinal cord injury was in T6 or higher
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At birth, the spinal cord has descended to:
L4
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What areas of the spinal cord are indicated?
A: dorsal column
B: Dorsal horn (sensory)
C: lateral corticospinal tract
D: lateral spinothalamic tract
E: Ventral horn (motor)
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what modalities does the DCML carry?
proprioception, vibration, and fine discriminative touch
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what modalities does the spinothalamic tract carry?
pain and temperature (and crude touch in the anterior tract)
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Risk factors for central cord syndrome
cervical spine stenosis and hyper-extension injuries
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What defines a complete spinal cord injury in an individual NOT in spinal shock?
No motor or sensory function at S4-5 level.
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A 28-year-old female patient with suspected multiple sclerosis is found to have a pale optic disk in the RIGHT eye. The swinging flashlight test reveals an afferent pupillary defect (Marcus Gunn pupil) when the light is moved from one side to the other.
What is likely to happen when the light is shone first in the LEFT eye and then moved quickly to the RIGHT eye?
Both pupils appear to dilate.
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What is the MAIN mechanism thought responsible for the beneficial effects of natalizumab in MS?
Reduces T-cell migration across the blood brain barrier
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In diseases such as MS, it is believed that the endothelial cells of the blood brain barrier
provide secondary signals for T cell proliferation.
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