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76 Cards in this Set
- Front
- Back
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what are the four classifications of motor unit diseases?
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1. polyneuropathy - diffuse peripheral nerve dysfunction
2. polymyositis - diffuse skeletal muscle dysfunction 3. junctionopathy - disorder of neuromuscular transmission 4. diffuse spinal cord disease |
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what is the major clinical sign of motor unit disease on physical exam? What are three neurological exam findings?
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- muscle atrophy and weakness
1. cranial nerve abnormalities 2. diminished or absent spinal reflexes 3. altered sensation if sensory nerves are involved |
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what are four ancillary aids that can be used to diagnose motor unit disease?
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1. electrophysiology
2. serum enzymes (CK, LDH, AST) 3. muscle and nerve biopsy 4. CSF tap |
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what are two neoplastic rule-outs for monoparesis?
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1. nerve sheath tumor
2. lymphosarcoma |
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what is one infectious rule-out for monoparesis?
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distemper neuritis (rare)
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temporary compression injury to a nerve is called what?
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neuropraxia
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cut axon, but connective tissue structure of the nerve remains intact is called what?
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axonotmesis
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a severed nerve is called what?
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neurotmesis
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define neuropraxia
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temporary compression injury to a nerve
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define axonotmesis
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cut axon, but connective tissue structure of the nerve remains intact
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define neurotmesis
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a severed nerve
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what is the rate at which axons grow?
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1-2 mm/day
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peripheral nerve trauma:
- clinical signs - diagnosis (3) - ancillary aids (3) - treatment - prognosis |
- CS: acute, NON-PROGRESSIVE loss of function
- Dx: motor loss, loss of sensation, muscle atrophy - AA: EMG, motor and sensory NCV - Tx: Sx, but rarely effective - Px: varies with severity of injury |
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suprascapular nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: C6-C7
- function: extension and lateral support of shoulder - cutaneous distribution: none - signs of dysfunction: little gait abnormality |
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axillary nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: C6-C8
- function: flexion of shoulder - cutaneous distribution: dorsolateral brachium - signs of dysfunction: little gait abnormality |
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musculocutaneous nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: C6-C8
- function: flexion of elbow - cutaneous distribution: medial forelimb - signs of dysfunction: little gait abnormality |
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radial nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: C6-T2
- function: extension of elbow, carpus, digits - cutaneous distribution: dorsolateral limb - signs of dysfunction: loss of weight bearing, unable to fix limb in extension |
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median and ulnar nerves:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: C8-T2
- function: flexion of carpus and digits - cutaneous distribution: palmar surface of paw, caudal forelimb - signs of dysfunction: little gait abnormality |
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sympathetic innervation to the face:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: T1-T2
- function: dilation of pupil - cutaneous distribution: none - signs of dysfunction: miosis, ptosis, enophthalmus (Horner's) |
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obturator nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: L4-L6
- function: adduction of pelvic limb - cutaneous distribution: none - signs of dysfunction: little gait abnormality; may slide laterally |
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femoral nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: L3-L6
- function: extension of stifle - cutaneous distribution: saphenous branch supplies medial thigh and digit - signs of dysfunction: inability to extend stifle |
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sciatic nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: L6-S3
- function: flexion and extension of hip - cutaneous distribution: caudal and lateral surfaces of limb - signs of dysfunction: cannot flex or extend digits and hock; cannot extend stifle |
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peroneal nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: L6-S3
- function: flexion of hock; extension of digits - cutaneous distribution: dorsal aspect of paw, hock, and distal limb - signs of dysfunction: cannot extend paw, therefore knuckles on dorsum; poor hock flexion |
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tibial nerve:
- spinal cord segments - function - cutaneous distribution - signs of dysfunction |
- spinal cord segments: L6-S3
- function: extension of hock, flexion of paw - cutaneous distribution: plantar surface of paw - signs of dysfunction: unable to fix hock in extension |
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what are 5 neurological exam signs of forelimb nerve root avulsion or stretch?
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1. radial
2. musculocutaneous 3. median and ulnar 4. Horner's 5. absent panniculus |
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what a complete brachial plexus nerve root avulsion, which part of the limb will have analgesia?
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- primarily distal to the elbow
- sensation to the shoulder area are from cutaneous nerves caudal and rostral to brachial plexus |
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describe the progression of a nerve sheath tumor
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slow, progressive loss of function in a limb
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what are some clinical signs on PE and NE of a nerve sheath tumor?
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- may feel palpable mass in nerves
- muscle wasting - pain - limb disuse - ± Horner's syndrome and spinal cord compression |
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how is a nerve sheath tumor treated and what is its prognosis?
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- Tx: remove tumor
- Px: guarded |
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what are two major categories of diseases that cause quadriparesis/quadriplegia?
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1. spinal cord disorders: upper motor neuron quadriparesis
2. motor unit disorders: lower motor neuron quadriparesis |
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How do you form a differential list for motor neuron disease that is caused by:
- neuropathy? - myopathy? |
- neuropathy: by history
- myopathy: by biopsy |
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who is most predisposed to chronic, insidious, anomalous peripheral neuropathies?
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young purebred dogs and cats
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metabolic peripheral neuropathies:
- onset time - reversibility |
- slow onset
- all are reversible |
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what are 6 metabolic causes of peripheral neuropathies?
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1. hypothyroidism
2. hypoglycemia / insulinoma 3. DM (cats >> dogs) 4. uremia 5. autoimmune diseases 6. paraneoplastic diseases |
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what is a typical history for acute polyradiculoneuritis?
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(Coonhound paralysis)
- 7-12 days after exposure to raccoon saliva is typical, but not absolute - any breed of dog |
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what is are clinical signs for acute polyradiculoneuritis?
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- ascending generalized lower motor neuron paralysis that may progress over 2-10 days to complete quadriplegia with cranial nerve involvement
- tail wag remains intact - spontaneous recovery occurs within 1 week - 3 months in most |
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what is the proposed pathogenesis of acute polyradiculoneuritis?
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- autoimmune to raccoon saliva that may have similar epitopes as peripheral nerve roots
- antibodies cross-link with myelin at nerve roots |
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what is the pathogenesis of myasthenia gravis that is
- congenital? - acquired? |
- congenital (very rare): reduced number of acetylcholine receptors on muscle
- acquired: antibodies against acetylcholine receptors result in functional reductions in their number |
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what are the three syndromes (forms) of acquired myasthenia gravis?
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1. focal form: face and esophagus only
2. intermediate form (most common): exercise associated weakness and megaesophagus 3. acute fulminate form: acute respiratory distress; death |
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what are two common complications of acquired myasthenia gravis?
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1. megaesophagus
2. pharyngeal paralysis - note: both can lead to aspiration pneumonia |
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what are 3 drugs commonly used to treat myasthenia gravis and their function?
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1. pyridostigmine bromine - AChE inhibitor
2. neostigmine - AChE inhibitor 3. steroids - ↓ immune response to autoantibodies → ↑esophageal motility → ↓ aspiration pneumonia |
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what is the prognosis of myasthenia gravis
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poor: 50% die from aspiration pneumonia due to megaesophagus
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what is the major caveat that must be taken into account when treating myasthenia gravis with AChE inhibitors such as pyridostigmine bromine?
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does not reverse megaesophagus. Need conservative management of this condition and wait until the autoantibodies subside
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chronic demyelinating neuropathy:
- onset time - reversibility |
- chronic, progressive onset or remitting and relapsing course
- irreversible |
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what is the signalment for chronic demyelinating neuropathy?
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- dogs and cats of any age and breed
- most common: dogs 1-14 years; cats < 1 year; geriatric cats |
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what is the etiopathogenesis of tick paralysis?
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- toxin produced by female Dermacentor tick
- blocks release of acetylcholine at the NMJ |
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what is the major clinical sign of tick paralysis?
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acute onset of generalized lower motor neuron paralysis; back legs first, then front legs
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how is tick paralysis treated? What is the prognosis?
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- remove all ticks and thus, the toxin source
- Px: good since CS typically resolve within 12 hours (neurotoxin does not bind irreversibly) |
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what is the mechanism of botulism toxin?
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irreversibly blocks the release of acetylcholine from the nerve terminal
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what are two main clinical signs of botulism?
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1. acute onset of generalized LMN quadriparesis
2. cranial nerve deficits (e.g. can't swallow) |
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how is botulism treated?
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polyvalent or type C antitoxin
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what is the prognosis of botulism
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good if treated: CS resolve in 4 weeks
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what is a potential complication of treating botulism with antitoxin?
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since it is derived from horses, it can cause anaphylaxis
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what are four metabolic DDx for myopathies?
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1. hypokalemia myopathy (cats)
2. Cushings 3. Hypothyroidism 4. Cachexia |
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what is a nutritional DDx for myopathies?
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Vitamin E / Selenium deficiency
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what are four infectious/inflammatory DDx for myopathies?
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1. Toxoplasmosis
2. Neospora Masticatory Muscle Myopathy 3. Myopathy associated with collagen vascular disorders 4. Myopathies associated with malignancies |
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comment on the etiology of Anomalous myopathies
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they are usually X-linked, autosomal recessive, or autosomal dominant inherited primary myopathies
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What are three genetic abnormalities that cause anomalous myopathies?
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1. membrane proteins (dystrophin or laminin)
2. ion channel (myotonia, malignant hyperthermia) 3. muscle metabolism (pyruvate dehydrogenase deficiency, lipid storage myopathy, etc.) |
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hypokalemic myopathy in cats
- clinical signs - diagnosis - etiopathogenesis - treatment |
- CS: acute onset of appendicular weakness, marked ventroflexion of the head and neck
- Dx: low serum potassium, high serum CK - TEX: unknown; possible excessive renal loss or decreased intake of potassium - Tx: potassium - oral best, IV if emergency; potassium gluconate elixir or powder |
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Myopathy due to Cushings Disease:
- pathophysiology - clinical signs - treatment |
(Hyper-A)
- atrophic myopathy with selective loss of type II myofibers - pseudomyotonia - responds to correction of underlying disease |
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what is the pathophysiology of hypothyroidism and cachexia in causing myopathy?
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selective atrophy of type II myofibers
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what are two common parasitic inflammatory myopathies?
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1. toxoplasma gondii
2. Neospora canium |
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myopathy due to toxoplasmosis or Neospora canium:
- clinical signs - diagnosis - treatment - prognosis |
- CS: multifocal neurologic disease; occasional cases have predominately motor unit signs; stiff-stifle syndrome seen in puppies < 4 months
- Dx: rising titers; biopsy; response to Tx - Tx: clindamycin; pyrimethamine and sulfadiazine - Px: varies with severity of CS. Extensor rigidity is not reversible |
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Masticatory Muscle Myositis:
- clinical signs - diagnosis - treatment - prognosis |
- CS: acutely, temporal swelling and pain on opening the mouth; chronically, atrophy of muscles of mastication and inability to open mouth
- Dx: muscle biopsy, MMM antibody titer - Tx: immunosuppressive therapy - Px: good to guarded, depending on the degree of fibrosis |
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what is the proposed etiopathogenesis of Masticatory Muscle Myositis?
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antigenically different myosins in muscles of mastication may be selectively targeted by immune reactions
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what disease has polymyositis associated with collagen-vascular disordered and malignancy as a major clinical sign?
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Lupus
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Malignant hyperthermia:
- in what five species has this been reported? - genetics? |
- humans, pigs, dogs, cats, and horses
- autosomal dominant trait |
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Malignant hyperthermia:
- pathophysiology - associated blood chemistry abnormalities - what can trigger an episode? - how is it diagnosed? - how is it treated? |
- defect in intracellular calcium homeostasis, resulting in intense muscle contraction
- hyperthermia, acidosis, and hyperkalemia are often associated - precipitated by exercise, stress, and halogenated gas anesthetic agents - Dx: halothane challenge test; in vitro caffeine and halothane contracture test - Tx: Dantrolene (decreases excitation-contraction coupling of myofibers); Iv fluids, steroids, bicarb, acepromazine |
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describe a genetic myopathic disease in Labrador retrievers
- age of clinical signs? - clinical signs - diagnosis - treatment |
- Exercise associated myopathy of Labrador Retrievers
- CS: begin at 7 months - 2 years of age; weakness progressing to collapse during strenuous exercise; most are normal after 10-20 minutes of rest - not a good way to diagnose or treat this disease except based on clinical signs |
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what are the 5 parts of the motor unit?
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1. ventral horn cell
2. peripheral axon 3. NM junction 4. muscle 5. sensory nerves |
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what are four clinical signs of motor unit injury?
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1. loss of motor function
2. rapid loss of muscle tone and bulk 3. loss of sensation if sensory nerves affected 4. loss of spinal reflexes |
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when a motor unit is injured, what can be injured? (3)
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- one nerve
- groups of nerves (i.e., brachial plexus) - all motor units |
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what is the basic pathway of a spinal reflex?
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nociceptor → dorsal root → interneuron → ventral root → motor neuron
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what happens to a spinal relfex if you sever an upper motor neuron to that area?
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exaccerated reflex
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what parts of the SC comprise the brachial plexus?
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C6 - T2
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what parts of the SC comprise the pelvic plexus?
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L4-S3
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