CNS- I

Question 1

What is multiple sclerosis?

Answer 1

Autoimmune demyelinating disorder

• inflammation and selective destruction of CNS myeline (brain and spinal cord)
  
  • autoreactive t-lymphocytes against myelin basic protein
  • antibodies against myelin oligiodendrocytic glycoprotein
• periphearl nervous system is not affected
• immune mediated response in genetically susceptible people
  
  • genetic and environmental factors (story about twins growing up in different climates. colder climate has higher likelihood of develping MS)
    
    • (1st degree relative, 15 fold increase in having disease)
  • HLA- DR2 haplotype have increased susceptibility

Question 2

What is the role of myelin in CNS?

Answer 2

• Provides high electrical resistance and low capacitance–> increases speed!
  
  • electrical insulator
  • critical to impulse transmission
• CNS myelination: by oligodendrocytes
• Myelin in CNS enables fast axonal conduction, energy conservation and space conservation
  
  • essential for survival of axons

Question 3

Pathophys of MS?

Where does the disease process mainly happen?

Answer 3

• Combination of inflammation, demyelination and axonal damage in CNS
• Demyelination of nerve fibers in white matter of brain, spinal cord and optic nerve
  
  • ​leads to decreased conduciton velocity and conduction blocks
• Lesions: hard, sharp edged demyelinated patches called “plaques” visible throughout the white matter of the CNS
  
  • plaques are end result of myeline breakdown
    
    • myeline breakdown is poorly understood
• Symptoms reflect areas of demyelinization in brain and spinal cord (every MS pt is different)

Question 4

What is the course of MS?

Answer 4

• inflmmatory period of about 2 weeks
  
  • period of pronounced, acute disability
• as inflammation subsides, pt starts to recover
• Combination of acute, subacute and chronic lesions
• 2 stages:
  
  • initial sequential develppment of small inflammatory lesions
  • later extension, consolidation of smaller lesions and scarring, plaques and ultimately long lasting, permanent dysfunction

Question 5

MS Signs and symptoms?

Answer 5

• Progressive
• periods of remission and exacerbation
  
  • eventually residual symptoms present even during remission
• spinal cord lesions: will see limb paresthesias, weakness, impotence, incontinence; ascending spastic paralysis (upper motor neurons)
• visual disturbancs: optic neuritis, loss of part of the visual field, diplopia
• Autonomic disturbances
• lack of coordination: involvement of cerebellum
• increased incidence of seizures
• cognitive and emotional disturbances
• increased body temperature causes exacerbation of symptoms

Question 6

What is Lhermitte sign? What is it a sign of?

Answer 6

Electrical sensation with neck flexion (sign of MS)

Question 7

What is relapsing/remitting MS?

Answer 7

• 85% of MS cases
• Discrete attacks over days to weeks with substantial or complete recovery over the ensuing weeks to months
• residual disability over time
• between attacks, patients are neurologically stable
  
  • some people go months/years without attacks

Question 8

What is secondary progressive MS? (SPMS)

Answer 8

• Begins as RRMS (relapsing/remitting MS).
• At some point, a steady deterioration in function unassociated with acute attacks occurs
  
  • great majority of RRMS ultimately evolves into SPMS
  • Seen as “late stage relapsing-remitting”

Question 9

What is primary progressive MS?

Answer 9

• Accounts for 15% of cases
• these patients do not experience attacks but only a steady functional decline from disease onset; disability develops faster
• (more serious)

Question 10

What is progressive/relapsing MS?

Answer 10

• These patients experience a steady deterioration in their condition from disease onset but experience occasional attacks superimposed upon their progressive course
  
  • exacerbation–> deterioration
  • (most severe form)

Question 11

MS diagnosis?

Answer 11

• No one definitive tests
• look at clinical signs/symptoms
• oligoclonal abnormalities in immunoglobulins, increased gamma globulin in the CSF
  
  • don’t expect immunoglobulin in CSF that’s not in blood
• Prolonged latency of evoked potential (decrease amplitude or delay)
  
  • secondary to slowing of nerve impulse conduction
• White matter changes on MRI brain- hyperintense lesions
  
  • can have a normal MRI with MS dx
• CT scan may be normal

Question 12

MS prognosis?

Answer 12

• Most patients with clinically evident MS ultimately experience progressive neurologic disability
• some MS patients have a benign variant of MS and never develop neuro disabiilty (~20%)
  
  • benign MS 15 years after onset are unlikely to have issues
• Pregnant MS patients experience fewer attacks during gestation (especially in last trimester) but more attacks in the first 3 months postpartum
  
  • immunosuppressed during pregnancy
  • after baby is born, first 3 months, woman is susceptible to attack of MS

Question 13

MS treatment?

Answer 13

No cure

3 arms of therapy

• 1) treament of acute attacks (glucocorticoids- IV and then oral taper)
  
  • no proof that coricosteroids prevent any long term damage or improve long-term outcomes
• 2) treatment with disease-modifying agents that reduce the biologic activity of MS: disease modifying agents, interferon- beta and others
  
  • interferon- reduces immune response and MS exacerbation, but make you feel like you have the flu constantly!
• 3) symptomatic therapy: address spasticity, pain, bladder dysfuction, depression, fatigue, sexual dysfunciton

Question 14

What is guillian-barre syndrome?

Answer 14

• Acute, life threatening polyneuropathy with an immune mechanism- unsure of exact etiology
• demyelination of multiple peripheral nerves
  
  • ​longest axons typically inovlved first: begins in the legs
  • may be motor, sensory or mixed
• ANS involvement possible- can be hemodynamically unstable. Risk of SCD.
  
  • postural hypotension, arrhythmias, resting tachycardia, facial flushing, abnormal sweating, urinary retention
• Lower motor neuron involvement: flaccid paralysis

Question 15

Pathophys of GBS?

Answer 15

• Uncertain: strong, but still inconclusive evidence that autoantibodies play an important role in GBS
• 70% of cases preceded by an acute infectious process (1-3 weeks earlier)
• strong evidence linking certain infections with GBS (campylobacter jejuni, CMV, EBC, mycoplasma pneumoniae)
• Theory- antigens create an immune response against nerve fibers and/or block presynaptic voltage-gated Ca channels and postsynaptic nAChR channels= NM weakeness
• complete spontaneous recovery is possible!
• rare association with immuniations
  
  • risk <1 per illion (higher risk of getting it following illness with the flu)

Question 16

GBS symptoms?

Answer 16

• Rapid, progressive limb weakeness and loss of DTR’s
• frequently preceded by an acute flu-like illness (2/3 of patients)
• paralysis begins in legs and ascends cephalad
  
  • bulbar involvement (old word for brain stem): bilateral facial paralysis (50% of those affected)
  • pharyngeal muscle weakness: difficulty swallowing
  • intercostal muscle paralysis: impaired ventilation
  • associated with pain/paresthesa
• ANS dysfunction can be life threatening
• May have SEVERE orthostatic hypotension
• high risk for VTE due to immobility

Question 17

GBS diagnosis?

Answer 17

• progressive, bilateral weakeness
  
  • starts in legs and then ascends
• >50% have burning, aching pain in back and thights
• areflexia (no reflexes)
• progression over 2-4 weeks
• symmetry of symptoms
• Cranial nerve inovlvmenet<– can affect CV, resp centers
• ANS dysfunction
• decreased nerve conduciton velocity
• NO fever

CSF: elevated concentration of protein in CSF with normal cell oucnts

• CNS often normal for 48 h after symptom onset

Question 18

GBS treatment?

Answer 18

• Time sensitive
• high-dose intravenous immune globulin or plasmapheresis: equally effective and one should be considered for all patient
  
  • needs to be started within 2 weeks of symptom onset. after myelin is degraded, not much help
• Supportive care
  
  • mechanical ventilation after vc <15 mL/kg and or ABG results indicate need
    
    • 30% will require vent support
  • Cuffed ETT/trach to prevent aspiration (weak pharyngeal muscles)
    
    • early consideration for trach is recommended
  • treatment of hyper or hypotension with meds (vasopressors, beta blockers, etc)

Question 19

GBS outcomes?

Answer 19

• 85% achieve full functional recovery
• 3-8% mortality
  
  • respiratory failure, sepsis, PE, cardiac arrest- ANS dysfunction
• segmental demyelination only- recovery in a couple of weeks
  
  • axonal connection remain intact
  • recovery is rapid as remyelination occurs
• Axonal degeneration- recovery incomplete and takes months
  
  • ​axons have degenerated and become disconnected from their targets (NMJ)
  • Must regenerate for recovery to take place
• 5-10% of patient with typical GBS have one or more late relapses

Question 20

What is parkinson’s disease?

Answer 20

• 2nd most common neurodegenerative dx, exceeded only by alzheimer’s disease
• disturbance in dopaminergic pathways b/w substantia nigra and basal ganglia
• mean age of onset is 60 years; frequency increases with aging

Question 21

Pathophys of parkinson’s disease? hallmark?

Answer 21

• Hallmarks: degernation of dopaminergic neurons in the substantia nigra
  
  • reduced striatal dopamine
  • intracytoplasmic proteinacous inclusions known as lewy bodies that primarily contain the protein alpha synuclein
• Clinical signs secondary to decreased produciton *70-80%) of dopamine in neurons of basal ganglia leading to the putamen and caudate nucleus
  
  • dopamine has inhibitory role in EPS
• Without dopamine, cholinergic neurons are unopposed, EPS motor symptoms devleop
• progressive disease over 10-15 years
  
  • death usually form fall or infection (r/t immobility)

Question 22

What are lewy bodies?

Answer 22

hallmark of parkinsons’s disease

• intracytoplasmic proteinacous inclusions that contain protein alpha synuclein

Question 23

Occurence of parkinson’s disease?

Answer 23

• Most cases (85%) offuce sporadically and have no known cause
• 15% familial: specific mutation and gene associations ahve been ID’ed
• NO environmental factor has been proven to cause parkinsons
  
  • association with TBI might make pt more susceptible
• Epidemiological associations
  
  • increased risk with exposure to pesticides, rural living and drinking well water
  • reduced risk with cigarette smoking and caffeine
• “double hit” theory: interaction b/w gene mutaiton that induces susceptibility coupled with expsoure to toxic environmental factor

Question 24

What is secondary parkinsonism?

Answer 24

• Can occur as a result of drugs, stroke, tumor and infection , or exposure to toxins such as carbon monoxide or manganese
• Drugs:
  
  • most common: dopamine blocking agnets such as the neuroleptics (used in psychiatry)
  • metoclopramide and chlorpromazine are also neuroleptic agents
  • other drugs: tetrabenazine, some CCB, amiodarone and litium

Question 25

What are some cardinal features of PD?

Answer 25

* bradykinesia * rest tremor * rigidity * gait disturbance/postural instability- *don't move arms when walking or don't turn head when turning body*

Question 26

What are other motor features with PD?

Answer 26

* Micrographia- *handwriting changes, small writing* * masked facies (hypomimia) * reduced eye blinking * soft voice (hypophonia) * dysphagia * freezing

Question 27

What are some nonmotor features of PD?

Answer 27

* Anosmia * snesory disturbances (pain) * mood d/o (depression) * sleep disturbance * autonomic disturbance * orthostatic hypotension * GI disturbance * GU disturbance * sexual dysfunction * Cognitive impairment (MCI/dementia)

Question 28

What is the mainstay of parkinson's treatment?

Answer 28

* Levodope * purpose: dopamine precurosr * prescribed in combo with peripheral decarboxylase inhibitor (carbidopa) * prevents preipheral metabolism ot dopamine * reduces N/V due to activaiton of dopamine receptors in the area postrema that are not protected by BBB and redices peripheral CV effects

Question 29

What is role of selegiline in parkinson's treatment?

Answer 29

* Type B MAOI * inhibit catabolism of dopamine in the CNS

Question 30

What is amantadine in PD?

Answer 30

* antiviral agent: MOA Unknown * used for advnaced dyskinesia

Question 31

What is role of COMT inhibitors in PD?

Answer 31

Increase elimination half time of levodopa to prolong effects

Question 32

What is the role of deep brain stimulation in PD?

Answer 32

* Head frame placement- MRI * Deep brain electrode through burr hold inot specific nuclei using fuduciary markings/microelectrode recordings * generator pakc implanted below clavicle or in abdomen

Question 33

What are some experimental treatments with PD?

Answer 33

* Gene therapy * stem cell injection * transplant of dopaminergic/adrenal meduallary fetal tissue

Question 34

What is alzheimer's disease? Duration of illness? Possible contibuting factors?

Answer 34

* Progressive degenerative d/o of the cerebral cortex, **especially the frontal lobe** * **poor prognosis** * typical duration of illness is 8 years. * death 2-5 years after onset of debilitating symptoms * #1 cause of dementai (60-80%) * #2 cause is vacular dementia (20-25%) * **Possible contributing factors** * **genetic patterns** * **beta-amyloid plaque** development (*also seen in normal elderly brain; more pronounced in AD)* * **inflammatory and oxidative stress processes** * role of **estrogen** in the brain- *women at higher risk than men* * *however, ​women who menstruate earlier or enter menopause later, have multiple pregnancies have decrased risk of AD*

Question 35

What is pathophys of Alzheimer's disease? 3 characteristic factors?

Answer 35

* Three characteristic features: 1. neurofibrillatory tangles- aggregates of highly phosphorylated tau proteins * tau protein- normally important structurally to neurons, but in alzheimers, the tau is hyperphosphorylated and accumulates in high concentration- however, no research has bene definitive 2. neuritic plaques- composed of degenerating axons and dendrites 3. neuronal loss - degeneration * **overprodcution or decreased metabolism of beta-amyloid peptide** leads to toic state causing degeneration of neutornal processes, neuritic plaque formation and eventually neuronal loss and clinical dementia * tangles and plaques cause neurons in brain to shrink and eventually die- **memory and language affected first** * **neuron degeneration leaves gaps** in brain's messaging network that may interfere with communication between cells * **additional changes in ACh and CNS** nicotinic receptors

Question 36

What are signs/symptoms in very mild Alzheimer's disease? Duration?

Answer 36

* AD begins in hippocampus in medial temporal lobe * Symptoms * short-term memory loss * (other health issues) * Duration 7-8 years

Question 37

What are mild and moderate symptoms of AD? Duration

Answer 37

* AD spreads to lateral temporal and parietal lobes (from hippocampus and medial temporal lobe) * Symptoms * readingmath problems * pood object recognition * poor direction sense * personal history memory loss * withdrawn socially * Duration: 2-3 years

Question 38

What are some moderately severe symptoms of AD? Duration

Answer 38

* AD spreads to frontal lobe * SYmptoms include * poor judgment * impulsiveness * short attention * need help with dressing * forget names of loved ones * may wander and get lost * Duration 2-3 years

Question 39

What are severe and very severe symptoms of AD?

Answer 39

* AD spreads to occipital lobe and cerebellum * Symptom include * vision problems * no coordination precision * can't dress self * incontinence * trouble speaking, eating * Duration 3-4 years

Question 40

AD treatment?

Answer 40

* Cholinesterase inhibitors such as tacrine, donepezil, rivastigmine and galantamine * memantine (Namenda) and other NMDA receptor antagonist- *thought we could slow process but has been disappointing* * behavioral therpay * NSAID * cholesterol lowering drugs * estrogen

Question 41

What are some causes of reversible dementia?

Answer 41

* **D**rugs and alcohol (esp anticholinergics) * **E**motions (eg depression) * **M**etabolic derangement (hypothyroid, electolyte abnormalities, end stage liver disease) * **E**yes and ears in decline * **N**ormal pressure hydrocephalus * **T**umor * **I**nfection (encephalitis, HIV, syphilis) * **A**nemia (eg vit b12, folate deficiency)

Question 42

What is lumbar spondylosis?

Answer 42

* Degenerative changes including disk disease, osteophyte formation, facet joint disease, and ligamentous laxity, which can cause stenosis, segmental instability and/or neuro deficiets- **most likely cause of back pain** * 95% of males and 80% of females aged \>65 yo show MRI evidence of LS

Question 43

What is lumbar canal stenosis?

Answer 43

* Decrease in total cross-sectional area of the spinal canal, lateral recess or neural foramen

Question 44

What is spondylolisthesis?

Answer 44

forward positon of 1 vertebral body in relation to the vertebral body below it

Question 45

What is spondylolysis?

Answer 45

congenital or degenerative/psottraumatic absence of the pars interarticularis between the superior and inferior articular processes, frequently associated with spondylolisthesis term used for stress fracture through the pars

Question 46

What is the lamina?

Answer 46

portion of arch that attaches ot vertebrae above and below via facet joints

Question 47

What is the pars articularis?

Answer 47

part of vertebral arch that connects these facet joints- it is the weakest part of the arch

Question 48

What is radiculopathy?

Answer 48

compression of a single nerve root

Question 49

Back pain occurence? frequent patho?

Answer 49

* 70% of adult population suffers from low back pain at some point during their lifetime * **spondylosis** is **most** **frequent** in the **cervical and lumbar spine,** the most mobile regions of spinal column * **lumbar canal stenosis** most commonly involves L4-L5 level, followed by L3-4 * **Lumbar spondylosis patho-** process of disk degerneration, bilateral facet joint arthropathy and osteophyte formation * facet joint cartilage destruction and capsular laxity can lead to subluxation and segmental lumba instability

Question 50

Non-surgical treatment of back pain?

Answer 50

* Conservative measures are helpful in most patients * NSAID * PT (spinal exercises, traction, heat/cold pack) * weight reduction * spinal epdiural/foraminal injection * facet joint injection * lumbosacral corset can be helpful for back pain due to instability

Question 51

What are some surgical methods to help with back pain?

Answer 51

* Indications for sx include cauda equina syndrome ( defect in bowel/bladder function, shooting pain down legs), progressive neuro deficits and severe unrelenting pain * **onset of bowel/bladder dysfunction is surgical emergency** * **severe canal stenosis:** decompressive sx (laminectomy, laminoforaminotomy, window laminotomy) of the stenotic segments * **fusion** considered for severe, unrelenting back pain d/t lumbar instability, **or** when stenosis requires complete excision of **more than 1 facet joint at a particular level**

Question 52

What is intervertebral disc herniation?

Answer 52

* Bulging of the nucleus pulposus (shock absorber b/w vertebral bodies) onto the spinal nerve * nerve root compression occurs when nucleus pulposus protrudes thorugh the posterolateral aspect or central aspect of the annulus fibrosis * radiculopathy causes pain in a single dermatomal distribution or localized weakness

Question 53

Common sites of intervertebral disc herniation?

Answer 53

* **LUMBAR**: Usually L4-L5 or L5-S1: low back pain, radiating down lateral/posterior thighs and calves (sciatica) * **CERVICAL:** Usually lateral protrusion at C5-C5 or C6-7 * C5-6: pain starts in neck, radiates to shoulder and down lateral arm to thumb * biceps muscles and reflex weak * C6-7: pain in scapula, triceps reigon and middle and index fingers

Question 54

Treatment for disc hernatiion?

Answer 54

rest pain contorl epidural coritcosteroids surgical decompresion

Question 55

What defines a spinal cord injury?

Answer 55

* Fracutre, contusion or compression of the vertebral column result in cutting, pulling, twisting, compression of spinal cord * usually trauma related * MVA 45%, falls 17%, acts of violence (ie gun violence) * Injury levels * Cpsine 55% (occurence) * tspine 30% * l-spine 15% * **Nontraumatic mechanism:** hyperparathyroidism; neoplastic lesions * **traumatic mechanism:** hyperextension, hyperflexion, vertical compression; rotation and shearing

Question 56

What do spinal cord injury symptoms depend on?

Answer 56

level of injury * Level of injury: the lowest spinal cord segment with intact motor and sensory function * loss of seonsory function within 3 levels of injury * hand paresthesias should raise concern for cervical injury

Question 57

Pathophys of spinal cord injury?

Answer 57

* Injury cuases **microscopic** **hemorrhages** in the gray matter and pia-arachnoid * **hemorrhage leads to necrosis** inthe gray matter and extend to white matter * spinal cord circulation is **impaired by edema** * edema and hemorrhage are **greatest at injury site. about 2 segments above and below** * **edema temporarily adds to patient's dysfunction** by increasing pressure and compressing nerves * **edema near C3-C5** vertebrae may interfere with phrenic nerve- impulse transmission to the diaphragm and **inhibit resp function** * In gray matter, an **inflammatory** reaction **prevents** **resoration** of circulation * phagocytes appear at the site within 36-48hours after injury, macrophages engulf degenerating axons, and **collagen replaces normal tissue** * scarring and meningeal thickening leave nerve in the area **blocked or tangled**

Question 58

What is a complete SCI?

Answer 58

* Loss of all sensory and motor function * reflexes intitially flaccis, but hyperreflexia develops over time * autnomic pathways are disrupted, resultingin urinary, rectal and sexual dysfunction * lose tone

Question 59

What are incomplete SCI syndromes?

Answer 59

* Brown sequard syndrome- hemisection of cord * Central cord syndrome * anterior cord syndrome * posterior cord syndrome * cauda equina syndrome

Question 60

What is brown-sequard syndrome?

Answer 60

* ipsilateral motor weakness and proprioception/vibration loss * contralateral pain and temp loss

Question 61

What is central cord syndrome?

Answer 61

* weakness of arms greater than legs d/t involvement of anterior horn cells. lmiited blader control may also result * pain/temp loss at level of injury * reflexes decreased in arms; normal to hyperactiv ein legs * frequently occurs wiht hyperextension injuries in elderly due to cervicla spondylosis * *happens in elderly with c spine injuries*

Question 62

What is anterior cord syndrome?

Answer 62

* weakness from involvement of coritcospinal tracts and anterior horn cells * disruption of spinothalamic pathways results in loss of pain, temp and light touch, with sparing of proprioception/vibration * reflexes intiially flacid, but hyperreflexia develops over time * autonomic pathways disrupted

Question 63

What is posterior cord syndrome?

Answer 63

* Motor pathways are intact * dorsal column impairment resulting in proprioception/vibration loss and a sensory ataxia

Question 64

What is cauda equina syndrome?

Answer 64

* Motor involvement results in rectal and bladder paralysis * sensory loss in area supplied by nerve roots * reflexes usually flaccid

Question 65

What is clinical course of someone with high tetraplegia SCI (C1-C4)

Answer 65

long-term vent support required

Question 66

What is clinical course of pt with C5 SCI level of injury?

Answer 66

Functional biceps allows greater independence through splinting and orthotics. generally able ot feed self and assist with upper body dressing

Question 67

What is clinical course of pt with C6 SCI injury?

Answer 67

Present of wrist extension allows use of tenodesis for greater hand use generally able to feed self and perform oral-facial hygiene

Question 68

What is clinical course of pt with C7 SCI?

Answer 68

Triceps funciton significantly increases independence most are independent with dressing and bowel, bladder management

Question 69

What is SCI treatment in acute injury SCI? Pain? DVT? Spastiicty? GI issues?

Answer 69

* **Acute injury** * keep systolic BP \>90 mmHg, use fluids or vasopressors for shock and hypotension * **Pain** * neuropathi pain: gabapentin, pregabalin, carbamazepine, phenytoin, tricyclics * MS pain: narcotics autely, NSAIDS * **DVT** * prophylaxis: enoxaparin 30-60 mg BID, sq heparin 5000 unit BID * Treatment: anticoag with heparin, then coumadin. if contraindicated, IVC filter necessary * **Spasticity** * useful drugs: gabapentin, baclofen, tizanidine, diazepam, dantrolene * intrathecal baclofen pumps helpful for excessiv espasticity * **GI issues** * ileus/gastirc motility: metoclopramide 10 mg QID, erythromycin * Ulcer prophylaxis: H2 receptor antagonists or sucralfate * Bowel porgram: adequat fluid, diet and activity level, stool softeners and blycerin/bisacodyl suppositiories

Question 70

What is neurogenic shock?

Answer 70

* autonomic reflexes **lost** in high/mid cervical injury disrupting sympathetic tone * **common with high thoracic and higher injury** * **decreased** peripheral vascular tone results in **expanded** **vascular space** and relative **hypovolemia**, with **hypotension**, **bradycardia**, and **warm, dry skin** * hypotension is result of : 1. **loss of sympathetic nervous system** activity and a decrease in systemic vascular resistance 2. **bradycardia resulting from loss of T1-T4 sympathetic** innervation to heart * These hemodynamic changes are collectively known as neurogenic shock and lasts **1-3 weeks** * monitor volume status carefully with appropriate use of vasopressors

Question 71

What is spinal shock?

Answer 71

loss of neurologic function * transient period of absolute flaccidity/atony, peripheral blood vessel dilation and reflex loss (decreased excitability) below lesion * duration 2-4 weeks * *spinal shock happens no matter where lesion is. neurogenic shock is sepcifically looking at impairment of T1-T4 sympathetic tone*

Question 72

What happens several weeks after SCI?

Answer 72

* chronic stage- after reflexes come back * overactivity of SNS * autonomic hyperreflexia (upper and lower motor neurons not talking) * involuntary skeletal muscle spasms * baclofen (potentiates GABA) is helfpul * can be given subarachnoid pump * must not be suddnely withdrawn: seizures * Benzos are helpful * spasiticty may be refracotry to pharmacological therapy * spinal cord stimulator * may require dorsal rhizotomy, myelotomy

Question 73

What is cause of autonomic hyperreflexia?

Answer 73

* Potentially life-threatening hypertensive condition that develops in up to 85% of pt with spinal cord injury above the splanchnic outflow, usually above level of T6 * noted in 45-85% of injuries at or above T6; onset \>6 months after injury * Triggered by afferent stimuli below the level of injury * distention of hollow viscera (bladder, uterus, gallbladder, bowel) * uterine contractions during obstetric delivery * cutaneous stimulation * surgical procedures involving pelvic organs or lower extremities *

Question 74

What is the pathophys behind autonomic hyperreflexia?

Answer 74

* CNS and upper spinal cord are isolated from spinal cord below the lesion * simulation below the spinal cord lesion- afferent impulse generated initiates a sympathetic reflex * this reflex is isolated from normal inhibitory "check and balance" system- profound vasoconstriciton below the lesion results * the carotid sinus senses the increased BP and causes a reflexive drop in SNS outflow above hte lesion- leaving PSNS "unchecked" above the lesion- bradycardia results profound/dangerous hypertension and reduced peripheral blood flow (too much SNS below the lesion) and bradycarida, cutaneous flushing and sweating (too much PSNS above the lesion)

Question 75

What are clinical manifestations of autonomic hyperreflexia?

Answer 75

* Marked hypertension * bardyacrdia * cardiac dysrhythmias * HA * piloerection * sweating * flushing above level of lesion * Severe HTN may lead to seizures or cerebral hemorrhage

Question 76

What is treatment for autonomic hyperreflexia?

Answer 76

* ID and treat underlying cause and treat HTN * Anti HTN- nitroprusside, hydralazine * PREVENTION IS BEST * Autonomic hyperreflexia can be prevented by either general or spinal anesthesia: both are effective in blocking afferent limb of the pathway

Question 77

What are SCI complications?

Answer 77

* Impaired alveolar vnetiation- lose of accessory muscles, especially when sick * autnomic hyperreflexia * chronic pulmonary and GU infection * renal stones: renal dysfunction * incomplete emptying of bladder, calculus formation * renal failure si major cause of death in SIC * Anemia * altered thermoregulation * Osteoporosis, skeletal muscle atrophy, skin breakdown * DVT risk * visceral pain from bladder/bowel distention * phantom pain in denervated areas * depression 25-50% * chemical dependency in up to 50%