Upper Vs Lower Neuronal Lesion Flashcards
Signs of Motor Neuron Lesions =
Paresis/Paralysis
Muscle atrophy
Involuntary mms contractions
Abnormal tone
Abnormal reflexes
Muscle hyper-stiffness
Disturbances of movement efficiency and speed
Impaired postural control
Central Nervous Signs/Sx =
Brain and Spinal Cord
Increased Tone
> Spasticity
> Rigidity
Clonus/Babinski
Increased Deep Tendon Reflexes
Atrophy over a prolonged period of time
Peripheral Nervous Signs/SX =
Outgoing/Input “Wires”
Decreased Tone/Flaccidity
No or diminished DTRs
Quick atrophy
Muscle tone =
Peripheral + Central Components
Normal Muscle Tone =Palpable stiffness (stretch resistance) in resting muscles
Low Muscle Tone =
hypotonia or flaccidity
LMN lesions
Acute UMN lesions (usually temporary)
Developmental disorders
High Muscle Tone =
Chronic UMN lesions
Some basal ganglia disorders
May be spastic or rigid
Abnormal Muscle Tone =
Brain is the mediator
Spinal Cord is the router
Peripheral nerves are just wires sending signals
No dampening of signals – increased tone, spasticity, rigidity, and a cycling of stretch reflexes
-Paresis =
A decrease in the amount of movement or strength
Hemi- One side of the body (R vs L)
Para- Caudal half (below arms)
Tetra*- All limbs
-Plegia (paralysis) =
A complete loss of the ability to move
Hemi-
Para-
Tetra*-
Formerly Quad-
What is Atrophy?
loss of muscle bulk
Denervated muscles demonstrate the most severe atrophy; even small, partial innervation will maintain some muscle fibers’ health
LMN damage results in rapid atrophy due to changes in the pattern of protein production
UMN damage = Muscles still receive stimulation from intact LMNs and atrophy is slower
Neurogenic atrophy:
due to nervous system damage
Disuse atrophy:
due to disuse
Types of Involuntary Muscle Contractions =
Abnormal movements due to basal ganglia dysfunction
muscle spasms
cramps
myoclonus
fasciculations
fibrillations
Muscle spasms =
Sudden, involuntary contractions of muscles
Cramps =
Particularly severe and painful muscle spasms
Myoclonus =
Brief, involuntary contractions of a muscle or group of muscles
May occur in a healthy nervous system or be signs of pathology (dependent on context)
Fasciculations =
Quick twitches of single motor unit muscle fibers that are visible on the surface of the skin
Fibrillations =
Brief contractions of single muscle fibers not visible on the surface of the skin
May occur with UMN or LMN disorders
Spinal/Cerebral Shock =
Occurs when UMN lesion disrupts descending motor command and results in a temporary inactivity of the LMNs
> Cannot elicit stretch reflexes, muscles are hypotonic
After recovery, interneurons and LMNs become active again but activity is no longer modulated by UMNs
Often in the months after UMN lesion muscle tone and stiffness increases within causing excessive resistance to muscle stretch
the differences between sensory losses at C7 and C8 =
Injury at ~C7 on (R)
Anterolateral spinothalamic tract
> Discriminative pain and temperature
> Fibers cross at spinal cord entrance
Impacting C7 fibers crossing anteriorly and those below after the decussation
> C7 (R) & below C8 (L)
Flushing =
Vasodilation
Miosis =
Dilator pupillae muscle paralysis (Muller’s) with pupil constriction
Ptosis =
Eyelid falling or drooping
Enophthalmosis =
Recession of eyeball in orbit
Presentation is like Horner’s Syndrome =
Would have anhidrosis
Autonomic Nervous System outputs =
Thoracolumbar – Sympathetic
Craniosacral - Parasympathetic
Innervation of visceral muscles and glands =
Cardiac muscles, lungs, secretory glands
GI tract - large portions of its innervation is localized
Parasympathetic Nervous System =
Homeostasis (Rest and repose #chillin’)
Sympathetic Nervous System =
Arousal (Fight or flight)
Cell bodies of the preganglionic neurons are located in the thoracic intermediolateral gray horn.
So, while the sympathetic paravertebral ganglia are physically intact, their neurons are impacted by the site of lesion because the artery involved also supplies the SNS ganglia.
