LMN Flashcards
LMN_GBS_Sp2025-student
what are the subsections of the peripheral nervous system?
somatic nervous system:
sensory division
motor division
autonomic nervous system
parasympathetic division
sympathetic division
Enteric nervous system
give some background on what lower motor neurons are?
Begin in the spinal cord
Innervate muscles and glands throughout body
Include cell bodies of motor neurons in the anterior horn of the spinal cord or,
What other chronic neurodegenerative disease affects the anterior horn cells?
motor neurons of the brainstem that contribute to cranial nerve motor functions and their axonal projections toward the periphery to innervate muscle
What is an example of a brainstem CN motor function?
Neurotransmitter at NM junction = acetylcholine (plus norepinephrine and epinephrine)
where is the site of session for a UMN injury vs a LMN injury?
UMN: cerebral hemispheres, cerebellum, brainstem, spinal cord
LMN: anterior horn cells, nerve roots, peripheral nerves, neuromuscular junction, muscles
what does muscle weakness look like for a UMN injury vs a LMN injury?
UMN: quadriplegia, hemiplegia, diapelegia, paraplegia
LMN: proximal(myopathy) and distal (neuropathy)
what does muscle tone look like for a UMN injury vs a LMN injury?
UMN: spasticity and rigidity
LMN: hypotonia
what does fasciculations look like for a UMN injury vs a LMN injury?
UMN: absent
LMN: present (particularly in the tongue)
what does tendon reflexes look like for a UMN injury vs a LMN injury?
UMN: hyperreflexia
LMN: hyporeflexia
what does abnormal reflexes look like for a UMN injury vs a LMN injury?
UMN: Absent (depending on the involved spinal levels)
LMN: present
what does sensory loss look like for a UMN injury vs a LMN injury?
UMN: cortical sensation
Cortical sensationrefers to sensation that requires some processing by the cortex to discriminate one stimulus from another. The cortical sensory modalities include graphesthesia, stereognosis, and the ability to perceive the presence of bilateral simultaneous sensory stimuli.
LMN: peripheral sensations
what does electromyography look like for a UMN injury vs a LMN injury?
UMN: normal nerve conductions and decreased interference patterns and firing rates
LMN: abnormal nerve conduction, Larger motor units, fasciculations and fibrillations
what structures are involved in the peripheral nervous system?
SC: anterior horn cell, spinal roots, peripheral nerves
how is tone presented in the peripheral nervous system?
Decreased/absent (hypotonia, flaccidity)
how do reflexes appear in the peripheral nervous system?
Decreased/absent (hyporeflexia)
Cutaneous reflexes decreased/absent
what involuntary movements impairments in the peripheral nervous system?
fasciculations
what is mononeuropathy?
muscles impacted from one nerve
what is Radiculopathy? what is an example?
muscles from a specific myotome- L4 DF/drop foot
what is polyneuropathy?
Polyneuropathy: Initially distal extremity muscles and progress to proximal muscles
what is special about the muscle bulk appearance in someone that has a peripheral nervous system session?
Neurogenic atrophy: rapid, focal, significant muscle wasting consistent with degree of axonal/myelin damage.
what so voluntary movements look like in a person with a PNS session?
Weak/absent
what is mononeuropathy?
Involvement of single nerve (cubital tunnel)
what is mononeuropathy?
Involvement of 2 or more nerves (bilateral carpal tunnel)
what is radiculopathy?
Involvement of nerve roots
what is plexopathy?
Involvement of brachial or lumbosacral plexus
what is polyneuropathy?
Involvement of 2 or more nerves
Generally, a result of a disease process affecting entire body
Associated with Diabetes Mellitus (diabetic neuropathy)
Associated with nutritional deficiency
Associated with chronic kidney disease (CKD)
what is neurapraxia?
demyelination of the nerve when the axon remains intact; weakness without atrophy expected; regeneration/remyelination probable
what is axonotmesis?
injury to the axon while the outer coverings of the nerve remain intact; Wallerian degeneration before regeneration occurs; weakness expected with atrophy
what is neurotmesis?
axon is severed, and the connective tissue coverings are disrupted; regeneration possible but not as effective; not likely to experience neurological recovery and need compensatory training for permanent loss
crushing injuries
how do PNI’s occur?
Traumatic injury to peripheral nerves is caused by contusion/compression, tension, ischemia, laceration, electrical source
what are the 9 causative factors of LMN sessions and PN lesions?
Physical injuries/trauma
Viral or bacterial infections
Autoimmune disorders
Uncontrolled diabetes
Genetic disorders
Certain medications (e.g. Thalidomide, statins, cardiac, chemotx drugs)
Nutritional deficits
Certain toxins (e.g. lead, arsenic, nitrous oxide, mercury), chronic ETOH
Unknown
how do you diagnosis LMN and PNI’s?
Neuro exam -> Clinical symptoms
Nerve conduction velocity test
Electromyography (EMG)
Spinal fluid analysis (looking for elevated proteins, normal cell count)
Blood and urine tests (R/O other disorders that can cause neuropathy, looking for unusual proteins)
MRI and CT Scans
what is chronic inflammatory Demyelinating polyneuropathy?
damage to the myelin sheath, immune system attack
progressive weakness, impaired sensation of U/LE
diminished DTRs
fatigue
unusual feelings in the body
what is the etiology of chronic inflammatory Demyelinating polyneuropathy?
CIDP can happen at any age; may be triggered by a viral infection; more common in young adult men
closely related to Guillain-Barrésyndrome; considered the long-term stage
what is the treatment for chronic inflammatory Demyelinating polyneuropathy?
corticosteroids, high dose IVIG, plasmapheresis
rehab/physical therapy
Corticosteroids (Prednisone, Prednisolone)are similar to naturally occurring anti-inflammatory hormones made by the body, and can be used as an initial treatment. Corticosteroids often improve strength, are conveniently taken by mouth, and are inexpensive. Side effects however can limit long-term use
High-doseIntravenous Immune Globulins (IVIG)is the only drug that has FDA, Canadian, and European approval for treatment of CIDP. IVIG contains naturally occurring antibodies obtained from healthy volunteers. IVIG is administered over the course of several hours.There are also newer treatments with preparations of higher concentrations that can be given subcutaneously now available for CIDP patients
Plasma Exchange (PE), or Plasmapheresis (PLEX),is a process by which some of the patient’s blood is removed and the blood cells are returned without the liquid plasma portion of the patient’s blood. It may work by removing harmful antibodies contained in the plasma
what is critical illness polyneuropathy and myopathy?
Acute or subacute axonal length-dependent neuropathy that occurs in critically ill patients, not as a direct consequence of their underlying illness
Increases ICU morbidity via the inability/difficulty in weaning these patients off mechanical ventilation
Increase long-term disability
Decreased exercise capacity and tolerance
Symmetrical paralysis
Associated with ARDS, sepsis, organ failure
what are the PADIS guidelines?
These PADIS guidelines provide an interdisciplinary roadmap for family/patient-centered, evidence-based care
ABCDEF
A= access, prevent and manage pain
b=spontaneous breathing trials
c= choice of anastenics and sedation
d= delirium
E early mobility and exercise
f= family involvement
what is the etiology for Guillain-Barre syndrome GBD?
Etiology: unknown; autoimmune mediated; usually occurs after recovery from an infectious illness (respiratory or gastrointestinal)
what is Guillain-Barre syndrome GBD?
Acute demyelination of cranial nerves and peripheral nerves/nerve roots
Acute inflammatory semylenation Polyneuropathy (AIDP)- sudden progression
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - slow progression
Acute, progressive, ascending weakness and sensory loss
Rapid onset, progressive- worst sxs in first 2 weeks from onset
Prognosis- most people FULLY RECOVER!
what are the signs and symptoms of GBS
Sensory loss, paresthesias (tingling/burning)
Motor paresis; relative symmetrical distribution; distal to proximal
Dysarthria, dysphagia, diplopia, facial weakness
what are the complications of GBS?
Respiratory impairment
Autonomic instability
Pain: myalgia
Risk of pneumonia
Prolonged hospitalizations and immobility (DVT, skin breakdown, contracture)
Relapse (rare- 1-3% of all cases)
what is the medical diagnosis for GBS?
- Lumbar Puncture: elevated albumin
- NCV: delays in latency
- EMG: decreased amplitude
what is the medical treatment for GBS?
Plasmapheresis
IVIG
what should you include in your examination for a patient with GBS?
Cardiac and respiratory status, vital signs
Cranial nerves (VII, IX, X, XI, XII)
Reflexes
Motor strength
Sensation
Functional status
what is the PT treatment for GBS?
PT Treatment Goals
Maintain respiratory function
Prevent indirect impairments- PROM, positioning, skin care
Prevent injury to denervated muscles- bracing, splinting, positioning
Muscle reeducation, moderate exercise program (active assist, AROM, progress to resistive with recovery, functional training as recovery progresses)
Patient and family education
Teach energy conservation techniques, activity pacing:
Avoid overuse and fatigue
what is Peripheral Nerve Disorder: Poliomyelitis Postpolio Syndrome (PPS)?
Slow progressive muscle weakness occurring in individuals with a confirmed hx of acute polio
Attacks cell bodies of motor neurons
20-40 years after initial attack (30-40%)
what re the common impairments of Poliomyelitis Postpolio Syndrome (PPS)?
Fatigue
Pain
Muscle weakness (asymmetrical)
Hypotonicity
what is the pt interventions for PPS?
Strengthening- be careful to avoid fatigue and muscle soreness
Aerobic capacity
Submax principles, low-mod intensity, frequent rest breaks
Whole body movements, focus on FUNCTION
Maintain respiratory function, energy conservation
Orthotics, DME
Research lacking
Moderate resistance with near normal strength;
Avoid muscle training with severe paresis
what is myasthenia gravis?
Postsynaptic neuromuscular junction disorder characterized by progressive muscle weakness and fatigability with exertion
Autoimmune antibody-mediated attack on acetylcholine receptors and NMJ
Acetylcholine receptors are destroyed
Prevents muscles from contracting
Course varies (may progress from mild to severe)
what are the signs and symptoms of Myastenia Gravis
fatigue or weakness with sustained activity
muscular strength worse with continuing contraction, improved with rest.
what are the 4 types of myasthenia?
1) ocular myasthenia (extraocular muscles)
2) mild generalization myasthenia
3) severe generalized myasthenia
4) crisis
what should be included in your PT examination for myasthenia gravis?
Cranial nerves (diplopia, ptosis, dysarthria, dysphagia, facial expression)
Ice pack test- positive test is decreased ptosis after 2 min application of an ice pack to affected eyelid
Muscle strength- proximal muscles more involved than distal
Fatigability- repeated muscle use results in rapid weakness
Functional mobility
what is the medical diagnosis for myasthenia gravis?
neuro exam
blood test (elevated antibodies)
EMG/NCV
CT/MRI
what is the pt treatment for myasthenia gravis?
Patient/family education
Safe functional mobility
Energy conservation techniques
Respiratory training
Muscle strengthening (2-3x/wk)
Include respiratory exercises
Moderate intensity (low with fatigue)
Focus on large, proximal muscle groups
Weight bearing activities
Balance training (1-2x/wk)
Aerobic exercise (low intensity: 30-50% VO2)
OT/SLP referral
what is the medical treatment for myasthenia gravis?
ace inhibitor
IVIG
corticosteroids
are the major takeaways of Evidence-Based Practice in Rehabilitation of Myasthenia Gravis. A Systematic Review?
Three different rehabilitative approaches were identified: physical training, respiratory training, and balance training.
All rehabilitative modalities contributed to enhanced functional outcomes, fatigue reduction, and improved QoL w/ moderate exercise intensity
Findings suggest the best approach likely a multidisciplinary one that combines physical, respiratory, and balance training
Bolded: No side effects have been linked to physical training in individuals with MG. However, it is suggested to restrict it to patients with mild to moderate symptomatology (stage IIA and IIB of the disease)
Currently cannot recommended one over another due to lack of cross-comparative studies
what are the key take aways from the article exercise therapy for muscle and lower motor neuron diseases?
Muscle and lower motor neuron diseases share a common denominator of perturbed muscle function, most often related to wasting and weakness of muscles. Currently there is no cure for these diseases.
Evidence indicates that moderate intensity aerobic- and strength exercise is advantageous for patients with muscle diseases, without causing harmful exercise-induced muscle damage.
On the contrary, motor neuron diseases show a rather blunted response from exercise training. High-intensity training is a modality that seems safe and a promising exercise method, which may circumvent neural fatigue and provide effect to patients with motor neuron disease.
Although we have come far in changing the view on exercise therapy in neuromuscular diseases to a positive one, much knowledge is still needed on what dose of time, intensity and duration should be implemented for different diseases and how to provide exercise therapy to very weak, non-ambulatory and wheelchair bound patients.
look over slide 35 and describe the differences between MS, myasthenia gravis and Guillian barre syndrome
