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Flashcards in CNS- I Deck (77)
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1
Q

What is multiple sclerosis?

A

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
2
Q

What is the role of myelin in CNS?

A
  • 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
3
Q

Pathophys of MS?

Where does the disease process mainly happen?

A
  • 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)
4
Q

What is the course of MS?

A
  • 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
5
Q

MS Signs and symptoms?

A
  • 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
6
Q

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

A

Electrical sensation with neck flexion (sign of MS)

7
Q

What is relapsing/remitting MS?

A
  • 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
8
Q

What is secondary progressive MS? (SPMS)

A
  • 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”
9
Q

What is primary progressive MS?

A
  • 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)
10
Q

What is progressive/relapsing MS?

A
  • 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)
11
Q

MS diagnosis?

A
  • 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
12
Q

MS prognosis?

A
  • 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
13
Q

MS treatment?

A

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
14
Q

What is guillian-barre syndrome?

A
  • 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
15
Q

Pathophys of GBS?

A
  • 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)
16
Q

GBS symptoms?

A
  • 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
17
Q

GBS diagnosis?

A
  • 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
18
Q

GBS treatment?

A
  • 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)
19
Q

GBS outcomes?

A
  • 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
20
Q

What is parkinson’s disease?

A
  • 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
21
Q

Pathophys of parkinson’s disease? hallmark?

A
  • 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)
22
Q

What are lewy bodies?

A

hallmark of parkinsons’s disease

  • intracytoplasmic proteinacous inclusions that contain protein alpha synuclein
23
Q

Occurence of parkinson’s disease?

A
  • 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
24
Q

What is secondary parkinsonism?

A
  • 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
25
Q

What are some cardinal features of PD?

A
  • bradykinesia
  • rest tremor
  • rigidity
  • gait disturbance/postural instability- don’t move arms when walking or don’t turn head when turning body
26
Q

What are other motor features with PD?

A
  • Micrographia- handwriting changes, small writing
  • masked facies (hypomimia)
  • reduced eye blinking
  • soft voice (hypophonia)
  • dysphagia
  • freezing
27
Q

What are some nonmotor features of PD?

A
  • Anosmia
  • snesory disturbances (pain)
  • mood d/o (depression)
  • sleep disturbance
  • autonomic disturbance
    • orthostatic hypotension
    • GI disturbance
    • GU disturbance
    • sexual dysfunction
  • Cognitive impairment (MCI/dementia)
28
Q

What is the mainstay of parkinson’s treatment?

A
  • 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
29
Q

What is role of selegiline in parkinson’s treatment?

A
  • Type B MAOI
  • inhibit catabolism of dopamine in the CNS
30
Q

What is amantadine in PD?

A
  • antiviral agent: MOA Unknown
  • used for advnaced dyskinesia
31
Q

What is role of COMT inhibitors in PD?

A

Increase elimination half time of levodopa to prolong effects

32
Q

What is the role of deep brain stimulation in PD?

A
  • 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
33
Q

What are some experimental treatments with PD?

A
  • Gene therapy
  • stem cell injection
  • transplant of dopaminergic/adrenal meduallary fetal tissue
34
Q

What is alzheimer’s disease?

Duration of illness?

Possible contibuting factors?

A
  • 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
35
Q

What is pathophys of Alzheimer’s disease?

3 characteristic factors?

A
  • 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
36
Q

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

A
  • AD begins in hippocampus in medial temporal lobe
  • Symptoms
    • short-term memory loss
    • (other health issues)
  • Duration 7-8 years
37
Q

What are mild and moderate symptoms of AD? Duration

A
  • 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
38
Q

What are some moderately severe symptoms of AD? Duration

A
  • 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
39
Q

What are severe and very severe symptoms of AD?

A
  • 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
40
Q

AD treatment?

A
  • 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
41
Q

What are some causes of reversible dementia?

A
  • Drugs and alcohol (esp anticholinergics)
  • Emotions (eg depression)
  • Metabolic derangement (hypothyroid, electolyte abnormalities, end stage liver disease)
  • Eyes and ears in decline
  • Normal pressure hydrocephalus
  • Tumor
  • Infection (encephalitis, HIV, syphilis)
  • Anemia (eg vit b12, folate deficiency)
42
Q

What is lumbar spondylosis?

A
  • 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
43
Q

What is lumbar canal stenosis?

A
  • Decrease in total cross-sectional area of the spinal canal, lateral recess or neural foramen
44
Q

What is spondylolisthesis?

A

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

45
Q

What is spondylolysis?

A

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

46
Q

What is the lamina?

A

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

47
Q

What is the pars articularis?

A

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

48
Q

What is radiculopathy?

A

compression of a single nerve root

49
Q

Back pain occurence? frequent patho?

A
  • 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
50
Q

Non-surgical treatment of back pain?

A
  • 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
51
Q

What are some surgical methods to help with back pain?

A
  • 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
52
Q

What is intervertebral disc herniation?

A
  • 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
53
Q

Common sites of intervertebral disc herniation?

A
  • 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
54
Q

Treatment for disc hernatiion?

A

rest

pain contorl

epidural coritcosteroids

surgical decompresion

55
Q

What defines a spinal cord injury?

A
  • 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
56
Q

What do spinal cord injury symptoms depend on?

A

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
57
Q

Pathophys of spinal cord injury?

A
  • 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
58
Q

What is a complete SCI?

A
  • 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
59
Q

What are incomplete SCI syndromes?

A
  • Brown sequard syndrome- hemisection of cord
  • Central cord syndrome
  • anterior cord syndrome
  • posterior cord syndrome
  • cauda equina syndrome
60
Q

What is brown-sequard syndrome?

A
  • ipsilateral motor weakness and proprioception/vibration loss
  • contralateral pain and temp loss
61
Q

What is central cord syndrome?

A
  • 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
62
Q

What is anterior cord syndrome?

A
  • 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
63
Q

What is posterior cord syndrome?

A
  • Motor pathways are intact
  • dorsal column impairment resulting in proprioception/vibration loss and a sensory ataxia
64
Q

What is cauda equina syndrome?

A
  • Motor involvement results in rectal and bladder paralysis
  • sensory loss in area supplied by nerve roots
  • reflexes usually flaccid
65
Q

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

A

long-term vent support required

66
Q

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

A

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

67
Q

What is clinical course of pt with C6 SCI injury?

A

Present of wrist extension allows use of tenodesis for greater hand use

generally able to feed self and perform oral-facial hygiene

68
Q

What is clinical course of pt with C7 SCI?

A

Triceps funciton significantly increases independence

most are independent with dressing and bowel, bladder management

69
Q

What is SCI treatment in acute injury SCI?

Pain?

DVT?

Spastiicty?

GI issues?

A
  • 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
70
Q

What is neurogenic shock?

A
  • 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
71
Q

What is spinal shock?

A

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
72
Q

What happens several weeks after SCI?

A
  • 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
73
Q

What is cause of autonomic hyperreflexia?

A
  • 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
      *
74
Q

What is the pathophys behind autonomic hyperreflexia?

A
  • 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)

75
Q

What are clinical manifestations of autonomic hyperreflexia?

A
  • Marked hypertension
  • bardyacrdia
  • cardiac dysrhythmias
  • HA
  • piloerection
  • sweating
  • flushing above level of lesion
  • Severe HTN may lead to seizures or cerebral hemorrhage
76
Q

What is treatment for autonomic hyperreflexia?

A
  • 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
77
Q

What are SCI complications?

A
  • 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%