Motor Systems Flashcards
Upper Motor Neuron Lesions: Weakness? Atropy? Fasiculations? Reflexes? Tone?
Weakness? Yes Atropy? No Fasiculations? No Reflexes? Increased Tone? Increased
Spastic paresis
+ Babinski
Lower Motor Neuron Lesions: Weakness? Atropy? Fasiculations? Reflexes? Tone?
Weakness? Yes Atropy? Yes Fasiculations? Yes Reflexes? Decreased Tone? Decreased
Flaccid paresis
Deep Tendon Reflex
(Monosynaptic): maintain muscle tone for posture
Ia afferent from muscle spindle activated–> excites alpha motor neurons of synergistic muscles and inhibits antagonistic muscles (reciprocal inhibition)
Use to detect hyper or hypoactive reflexes
- Decreased reflex: indicates disease of muscle, nerve or spinal cord
Increased reflex: indicates loss of descending inhibitory input to LMN
Flexor Reflex
Flexion and crossed extension reflex (polysynaptic)
Role: withdraw from a painful stimulus
Stimulus: activation of nociceptors
Spinal cord: activation of interneurons that excite ipsilateral flexor muscle and inhibit extensr (withdraw leg) AND activation of interneurons that cross spinal cord and excite contralateral extensor muscle and inhibit contralateral flexor muscle (maintain support for standing)
Golgi Tendon Reflex
Inhibits alpha motor neuron (via inhibitory interneuron)
- Role: Precisely control fine adjustments in muscle contraction
- Stimulus: tension on GTO activates Ib inhibitory interneurons (as well as input from cutaneous, joints and descending pathways)
- -> inhibits original muscle that was stretched
Muscular Dystrophies
Myopathy: Abnormality of the muscle
- Chronic, hereditary disease
- symptoms caused by muscle weakness
Duchenne’s: common in children (wasting, weakness in pelvic muscle)
Cause: lack of gene for dystrophin
- x-linked, recessive
- disease progressives with age, death 20-30 from respiratory complication
Sx: lordosis, muscle wasting of pelvic girdle muscle, scoliosis, gastroc shortens so muscle appears enlarged, high CK levels
+ Gowers (push up from ground slowly)
Myasthenia Gravis
Pathophysiology: autoimmune disorder that impairs transmission at NMJ
d/t antibodies made against nicotinic acetylcholine (AcH)–> reduced amplitude of end plate potential, AP fails to fire, Ach depleted with repeated firing–> muscle power is reduced–> fewer muscle fiber contract
Sx: Fatigue, weakness in cranial muscle, eyelids, eye muscles, ptosis, speech difficulty, difficulty chewing, difficulty breathing, weakness in arms and hands
Tx: Acetylcholinesterase inhibitors, plasmophoresis (removes antibodies to Ach R)
Amyotropic Lateral Sclerosis (Lou Gehrig’s)
Disease of corticospinal tracts
- Carry axons of pre-motor cells
- Loss of MN in ventral horn of spinal cord
- Loss of motor nuclei in lower brainstem
- Degeneration of corticospinotracts
- Loss of Betz cells and pyramidal neurons
Spares ocular muscle, voluntary control of bladder sphincters
Sx: combined upper and lower motor neuron signs
LMN: progressive weakness, atrophy, fasiculations
UMN: spasticity, hyperreflexia, Babinski’s sign
Dysarthria, Dysphagia, Respiratory muscle weakness and failure, head droop (weak neck muscles)
Emotional incontinence: lesion in corticobulbar pathway
Guillain-Barre Syndrome
Acute inflammatory demyelinating polyneuropathy.
Patients often have near full recovery (onset 1-2 weeks after viral infection- inappropriate activation of immune sys)
Sx: Tingling of hands and feet (crawling skin), difficulty getting out of chair
Rapid onset of weakness in legs and arms, weakness and paralysis of breathing muscles, eye and face. Severe cases: patients may be paralyzed. Loss of stretch reflex.
Tx: plasmaphoresis and reinfusion
Benedikt’s Syndrome
Unilateral lesion of red nucleus
Occulomotor palsy
Contralateral tremor
Decorticate Posturing
Upper Midbrain damage: patient exhibits
Patient exhibits upper limbs flexed at the elbow, lower limbs extended
“to the core”
Decerebrate Posturing
Patient exhibits extension of upper and lower limbs
- increased muscle tone
- removes excitatory input to inhibitory LRST
- ascending input is intact
Parinaud’s syndrome/ Dorsal midbrain syndrome/ Collicular Syndrome
Lesion in superior colliculi or posterior commisure:
- impaired vertical gaze
- large, irregular pupils (do not constrict with light)
- ptosis
- convergence/retraction nystagmus (attempted upward gaze–> eyelids oscillate between convergence and retraction)
Cause: pineal gland, hydrocephalus
Lateral Medullary Syndrome of Wallenberg
Cause: Vertebral artery or PICA
-Ipsilateral: dysphagia and dysarthria (Nucleus ambiguus), loss of pain and temperature from face (spinal tract of V), vertigo, nausea, nystagmus (vestibular nuclei)
Contralateral: loss of pain and temperature
“checkerboard pattern”
Pseudobulbar palsy
Cause: bilateral lesion of corticobulbar tract d/t brainstem infarct, ALS, MS
Sx: Dysphagia, dysarthria, paresis of the tongue, loss of emotional control
Bell’s palsy
LMN lesion of CNVII
(peripheral VII)
Ipsilateral paralysis of the face
Central VII lesion
UMN lesion of corticobulbar tract
Contralateral paralysis of lower quadrant of face
Tongue deviates away from lesion
Contralateral Corticonuclear tract
Tongue deviates towards lesion
Peripheral lesion of CNXII
Dysfunction of the cerebellum
- Signs are: Ipsi or contra?
- Major signs?
Cerebellar lesions are Ipsilateral.
Major signs: ataxia, hypotonia, intentional tremor, dysdiadochokinesia, dysmetria, nystagmus.
Can impair motor learning
Dysfunction of the basal ganglia
Usually due to a disruption of NT release
Abnormal movements are commonly cased by release of system from inhibition
Sx:
- Involuntary movements: tremor at rest, athetosis, chorea, ballism, dystonia
- Akinesia and bradykinesia
- Changes in posture and muscle tone
- Muscle rigidity
Parkinson’s Disease
Degeneration of dopaminergic cells in SNc (Substantia Nigra pars compacta)
Sx: tremor at rest, rigidity and bradykinesia hypokinetic movement disorder 1. Resting tremor 2. bradykinesia 3. rigidity 4. postural instability
Pathology:
-Direct: SNc does not release DA–> does not inhibit striatum–> Does not inhibit GPi/SNr–> Inhibits Thalamus–> inhibits movement
-Indirect: SNc does not release DA–> activates striatum–> activates STN–> activates GPi/SNr–> releases GABA–> thalamus is inhibited–> inhibits movement
Huntington’s Disease
Degeneration of cholinergic and GABAergic neurons in striatum d/t lesion in the caudate
- removes inhibition of GPe–> activation causes GPe to release glutamate–> activates GPi/SNr–> activates Thalamus–> facilitates movement (hyperkinetic)
- inherited ( CAG repeats in chr. 4)
- Chorea, athetosis and dystonia
Tardive Dyskinesia
Results from long term use of anti-psychotics which block dopamine transmission
Sx: involuntary movements (esp. of face and tongue)
