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decreased muscle function, flaccid
- -injury btw brain and SC
- -or injury with the SC itself before the anterior horn synapse
- -result is spastic paralysis (lack of inhibitory input)
- -ex: CP
- -injury below the SC (below L1)
- -injury btw SC and the muscle or below synapse at anterior horn
- -primary muscle or peripheral nerve injury
- -result is flaccid paralysis
Injury to what areas would cause an UMN injury?
Motor cortex, brain stem, internal capsule, SC
Injury to what areas would cause a LMN injury?
Anterior horn cell, primary muscle, myoneural junction, bulbar area
- LMN injury (even though it's in the brainstem)
- injury to CN 9, 10, and 12
- s/sx paresis or paralysis of the jaw, face, tongue, and pharynx
Is damage to the extrapyramidal tract considered UMN or LMN?
What 2 types of motor function make up extra pyramidal syndromes?
- 1) basal ganglia (imbalance btw Ach and dopamine)
- 2) cerebellum (difficulty coordinating voluntary movement and gait)
What effect does excess Ach in the basal ganglia have?
hypokinesia or akinesia
What effect does excess dopamine in the basal ganglia have?
How does injury to the extra pyramidal tract differ from injury to the pyramidal tract?
- Extra pyramidal tract injuries cause movement disturbance WITHOUT paralysis
- Get hypo or hyperkinesia
Damage to pyramidal tract (corticospinal tract) causes paralysis
- Orthostatic hypotension
- Labile BP
- High resting HR
- Cardiac conduction abnormalities
Why do pts with dysautonomia require direct acting pressors?
- There is an altered amount of NT in the presynaptic vesicle, an indirect acting drug causes an erratic response. Ephedrine may cause a large or small release of the NT (NE).
- Hence we give Neo (direct acting).
Patho of PD
- Insufficient quantity of dopamine in the basal ganglia
- Relative increase in the amount of Ach
- akinesia and tremor
- ANS dysfunction
- levodopa to increase dopaminergic activity
- anti-cholinergics (cogentin)
PD meds intra-op- d/c or continue?
Anesthesia drugs to avoid with PD
Droperidol and reglan (dopamine antagonists)
- Relative increase of dopamine in the basal ganglia
- Relative decrease of Ach
- Opposite of PD
Patho of MS
- demyelination of axons causes abnormal nerve conduction
- autoimmune disease affecting the CNS
- 2 x as common in women vs. men
Progression of MS
inflammation to demyelination to axonal damage
Anesthesia considerations r/t MS
- ANS dysfunction
- Steroid use (stress dose steroids)
- Concern for post-op weakness
- Avoid temp increase!!!!!
Anesthesia considerations r/t PD
- Propofol will decrease PD tremors
- Treat hypotension with direct acting pressor (ANS dysfunction)
- ANS can cause venous pooling so keep pt volume loaded
Considerations r/t pts with NM disorders
- degree of weakness
- degree of atrophy affects the number of extra-junctional receptors
- may want to avoid succ (excess K release) if there's paralysis or significant weakness
Regional anesthesia considerations r/t MS
- Avoid spinal (maybe implicated in post-op complications 2/2 LA toxicity)
- Caution with LA as BBB may be more permeable (myelin serves to protect the nerves)
- Epidural anesthesia is ok
charot marie tooth
- similar to MS
- demyelinating disease
ALS (amyotrophic lateral sclerosis) patho
- motor neuron disease affecting both the UMN and LMN
- involves both the pyramidal tract and the anterior horn of the SC
- may also involve the bulb of the brain stem
- most commonly affects men 40-60 yo
progressive skeletal muscle weakness, atrophy, and paralysis
Anesthesia considerations r/t ALS
- -degree of respiratory involvement
- -aspiration risk- bulb involvement may cause dysphagia
- -risk for hyperkalemia from such due to muscle wasting
- -sensitivity to NDMR
Regional anesthesia with ALS
Generally avoided due to fear of disease exacerbation and medical legal risks
Friedrichs ataxia patho
- similar to ALS as it also affects both UMN and LMN
- degeneration of spinocerebellar and pyramidal tracts
Friedrichs ataxia s/sx
- CMP in 10-50% of pts
- Kyphoscoliosis in 80% of pts (causes a rx lung disease)
- slowly progressing SC degeneration
- found in newborns
- abn of embryological development
- found in newborns
- degeneration of the bulb in the brain stem
major issue with syringomyella and syringobulbia
- -CSF outflow obstruction from the 4th ventricle
- -due to obstruction thru foramen of magendie and lushka into the cisterna magna
- cause unknown
- preceded by a virus in 70% of pts
- LMN involvement
- flaccid paralysis
- can vary from leg paresis to total motor paralysis
- bulbar involvement and pharyngeal muscle weakness
- ANS dysfunction
- may resolve or may have permanent damage
Recommendations re: NMB with pts with severe NM disease
- avoid succ!!
- avoid NMB if possible
- use smallest possible dose of NDMR and use peripheral nerve stimulator
What drugs must be avoided with porphyria
- disease of muscle, not nerves
- chronic autoimmune disease caused by destruction of Ach receptors
- pt develops antibodies to their own Ach
- origin of antibodies unknown but the thymus plays a role
- bulbar muscles often involved
If a pt is scheduled for removal of the thymus gland what disease would you be suspicious for?
- anti-acetylcholinesterase drugs to increase Ach levels
- PO pyridostigmine (increases amt of Ach at NMJ)
- pt has decreased number of Ach receptors so thus need more Ach at the site
- immunosuppressants to decrease antibodies
NMB considerations for MG
- More sensitive to NDMR (still need neostigmine for reversal)
- Resistant to succ (takes more to paralyze them) and long DOA
- Avoid NMB
- If must use NMB give 2/3 dose of NDMR and use a nerve stimulator
Why is the DOA of succ increased with MG?
Pts take anti-cholinesterase drugs which also decrease the amount of pseudocholinesterase
- resembles MG
- treatment with anti-acetylcholinesterase drugs NOT effective
- often associated with SC lung ca
- not a nerve issue but a muscle issue
- painless degeneration and atrophy of skeletal muscle
- ? mutation of dystrophin gene on X chromosome
- this results in the muscle being more permeable to Ca++
- this leads to muscle cell breakdown (resembles MH)
Anesthesia considerations for MD
Avoid triggers like succ and volatiles!!
- contracture of skeletal muscle after muscle stimulation ceases
- hallmark sign is inability to release handgrip
- due to abnormal Ca++ metabolism
- result is degeneration of skeletal muscle
- type of myotonic dystrophy
- these pts are susceptible to MH
What can precipitate muscle contraction with Steinert's disease?
- anti-acetylcholinesterase drugs
- cold T and shivering
- surgical manipulation
What would you like to do?
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