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197 Cards in this Set

  • Front
  • Back
Decreased body movement
Slow body movements
loss of ability to preform previously learned purposeful motor act in the absence of any overt primary motor or sensory loss
reduced spontaneous movements
meaning “dance” in Greek, this refers to random, purposeless, jerky movements
abnormal postures, usually associated with movements, typically turning in nature, caused by
co-contraction of agonist and antagonist muscles
a regular, large amplitude jerk or series of jerks, slower than myoclonus, associated with
spasticity or seizures
What muscle is voluntary? Involuntary?
Striated or Skeletal
Smooth and Cardiac
What is the neurotransmitter used with muscles?
What is a high safety factor?
1:1 relationship between AP in motor axon and contraction of muscle fiber
Differences between slow and fast muscle
Fast: large, rapid fatigue, anearobic (glycolytic), produces short forceful contractions.
Slow: small motor units, slow fatigue, oxidative lipid metabolism (lots of mitochondria and rich capillary supply)
LMN is a _____motor neuron
Each muscle fiber has innervation from ___ motor neuron, with the exception of _____
1 motor neuron, extraocular muscles
What is a motor neuron pool?
all alpha motor neurons innervating one muscle.
Difference between fibrillations and fasciculations.
Fasculation: UPM. Can be seen by eye. Spontaneous discharge
Fibrillation: LMN. Deinnervated muscle (from death or interruption of an axon), can't be detected visually
How does the CNS control muscular contraction?
Number of alpha motor neurons (recruitment of small fibers first)
Firing rates
Golgi tendon organ is a _____?
Golgi tendon senses _____ through what type of fiber?
Force, IB ----> spinal cord
Sensitive to contraction of a small number of motor units
Insensitive to passive strethc
Muscle spindle senses____? Via what kind of fibers?
Ia (velocity) and II (length) ----> CNS
Intrafusal fibers are what? Innervation>
small fibers of the spindle (Gamma innervation)
Extrafusal fibers?
Outside spindle
Alpha motor neurons
Two ways to make Ia fire stronger:
1)Muscle stretch of annulospinal endings of Ia, which increase Ia firing rate of the axon
2) Gamma neuron discharge, which increase Ia activity even when intrafusal fiber is fixed at both ends and length doesn't change
How do gamma neurons work?
stimulation of a γ-motoneuron from higher centers (gamma contracts the ends of the intrafusal fibres and consequently stretches the middle part of the muscle spindle. This part of the spindle is innervated by type Ia sensory fiber that go on to synapse with alpha-motoneurons, completing the gamma-loop.
Do intrafusal fibers generate APs? Do they contribute to the force of a muscle
No, they do not generate AP or twitch.
No, they do not contribute directly, but instead help keep sensory receptors sensitive to stretch. Gamma fibers can vary overall length of intrafusal fibers and can increase impulse traffic in Ia by stretching equatorial region
What is alpha-gamma coactivation?
It when gamma and alpha are activated together such that extra and intrafusal fibers contract and expand together.
Ia axons are found in what part of the spindle? What do II fibers do?
equatorial region of intrafusal muscle fiber
II fibers report steady state length of a muscle
What is the gamma loop?
gamma activation --> intrafusal shortening --> Ia activation ---> alpha activation ---> extrafusal contraction
High gamma motor neuron activity can lead to
hyperreflexia: increased sanity of the gamma loop to muscle stretch
How does one cure rigidity caused by gamma motor neuron increased firing
cut dorsal root (where gamma mn enter)
What is the motor neuron organization in the spinal cord?
axial and proximal mn are found medially
distal mn are found laterally
Describe a monosynaptic reflex
-Ia and alpha motor neuron on Homonymous muscle.
-Reciprocal innervation (Ia inhibits neurons of antagonist va inhibitory interneuron
-segmental sensory and motor function test
What is the Hoffman reflex?
test mytotatic stretch reflex electronically to distinguish central and peripheral processes.
M wave (first) indicates direct muscle activation
H wave: Ia afferent reflex, shows that Ia afferent, motor neuron and synapse all work
What is the Jendrassik's maneuver?
increases gamma neuron activity via propriospinal pathway. When pulling your hands apart you get larger reflex.
what happens when you increase load?
increase stretch, increase firing of Ia afferents, increase firing of motor neurons
what is spasticity?
increase in resting motor tone
increase in reflex excitability
If you cut the dorsal horn to treat spasticity and it is not successful, what does this indicate?
Excitability not due to Ia afferent input
How does the flexor and extensor reflex work
You get ipsilateral flexion and contralateral extension.
On the side with pain ---> extensors inhibited and flexors activated
On side without pain---> extensors activate and flexors inhibited.
When would you see spontaneous crossed extensor reflex?
in babies. goes away around 3 months of age.
What are the three major descending motor pathways?
1) Ventromedial pathway (tectospinal, vestibulospinal, and reticulospinal).
2) Lateral Brainstem Pathway (rubrospinal)
3) Corticospinal pathway (pyrimidal)
What pathway goes through the midbrain tectum? What does it control?
Tectospinal - Axial muscles
What pathway goes through the red nucleus
Lateral brainstem pathway --> rubospinal pathway
Does girdle and proximal upper limb muslces
What pathway has its nucleus in the medulla?
Vestibular and Reticular (medulla + pons)
They both operate on axial muscles
What tracts do not decussate?
reticulospinal and rubrospinal
Reticular formation has what function?
keeps you awake!
What tracts send projections bilaterally?
vestibulospinal and tectospinal.
Decorticate rigidity vs decerebrate rigidity
Decorticate: large lesions of cerebral cortex, extension of legs and flexion of arms (bc rubropsinal pathway intact)
Decerebrate: midbrain lesion, vestibulo/reticulospinal tracts unregulated ---> activation of leg and arm extensors
Possible causes of decerebrate rigidity
syrinx (cystic cavity) around ventricle in the brainstem or central cord of spinal cord
Basilar occlusion
Locked in Sydnrome
Bilateral pontine lesions (basilar artery infarct or hemorrhage)
No motor but spared cognition and sensation
Only can move eyes vertically bc CN III in midbrain is intact.
What is the role of the premotor cortex and supplementary motor cortex
Area 6 (premotor is lateral and supplementary is medial).
Motor planning.
Imagining a movement.
What are the inputs to the Motor Cortex?
1) VL thalamus (with connections to Basal Ganglia and Cerebellum, MOTOR CONTROL
2) Somatic Sensory input (VIA VP Thalamus)
3) Higher cortical areas (association areas, prefrontal cortical areas)
4) Modulators: Brainstem diffuse transmitter systems mostly from brainstem nuclei
Outputs of motor cortex
1) to motor controls structures: Basal Ganglia, Pons and Corticospinal tract
2) Output to its own input systems ---> VL Thalamus, Association Cortex
3) Output to Sensory Relays (somatic sensory cortex)
SMA, PMA, or Posterior Parietal Lesions
No paralysis or weakness
Apraxia: loss of ability to preform previously learned, purposeful motor act in absence of any overt primary motor or sensory loss
Neglect syndromes results from what?
Posterior parietal legions
Supranuclear lesion of Cranial Nerve VII
can move forehead but not lower half of face, sign of a stroke
Upper face is special, why?
It has dual innervation via corticobulbar tract
When we are learning a task, we do what
recruit motor neurons
What artery supplies the internal capsule
Internal Carotid
Middle Cerebral
Basal ganglia is supplied by what vessel?
Name the parts of the Basal Ganglia
Globus Palladus (Internal and External)
N. Accumbens
Substantia Nigra
Subthalamic Nucleus
Does the Basal Ganglia have a direct connection to the cerebral cortex?
NO! Output is two the VL nucleus of the thalamus.
What part of substantia nigra has dopamine cells lost in parkinsons
pars compacta
Basal Ganglia Loop is INhibitory or excitatory
Describe the indirect tract in Basal ganglia
Striatum inhibits external globes pallidus, which decreases inhibition of Subthalamic nucleus, which increases activation of Gpi, which increases inhibition of thalamus, which decreases cortex activity
Describe direct loop
Striatum inhibits Gpi, which decrease inhibition of thalamus which increases activation of cortecx
What modulates the Basal Ganglia
Substantia nigra (Dopamine)
What are the three loops of the Basal Ganglia
Sensorimotor ---> Putamen (Movement)
Prefrontal ---> Caudate (Memory)
Limbic ---> Accumbens (Mood)
Abnormal resting muscle tone
Involuntary or Abnormal movements
Basal Ganglia lesion signs
Dyskinesias (akinesia, bradykinesia, tremor, chorea, athetosis, Ballism, blepharospasm)
What is Ballism
involuntary flinging of the extremities, usually unilateral.
Cause: Less Gpi Excitation, less inhibition of thalamus
Cerebellar peduncle paths
Superior --> Output
Middle---> inputs pontine projections
Inferior ---> inputs from inferior olive
Outputs of Superior Cerebellar Peduncle
Fastigial nucleus ---> Vesticular and reticular nuclei
Interpositus nucleus --> Red Nucleus
Dentate Nucleus ---> Thalamus (cortex)
What is an intention tremor
nearer to target. Increases on movement
what is the first sign of midline cerebellar tumors
truncal ataxia
lateral lesions of cerebellum affect what?
Movement of limbs
Do more axons enter or leave the cerebellum?
Ipsilateral cerebellar hemisphere connects to ___ cerebral hemisphere
Which spinal tract does a double decussation
Rubropsinal tract (R. Interpossitus nucleus--->L. red nucleus ---> Right spinal cord
How do the cerebllar cortex and deep nuclei interact?
The cerebellar cortex exercises a veto over every pattern but the correct one....so its inhibitory.
that way the deep nuclei transmit the correct pattern of excitation to the cell targets
Mossy fibers are:
In cerebellum. Mostly input axons
Have collateral that excite cells in the deep nuclei
Excite granule cells ---> giver rise to a single axon that rises to cortical surface and splits to form a Parallel fiber---> which contacts 1000s of purkinje cells
Climbing fibers
From inf. Olive nucli
give off collaterals to deep cerebellar nuclei
Send out tendrils along dendrites of purkinje cells to excite them
One purkinje cells gets excited by only one climbing fiber but a climbing fiber can innervate more than one perkinje cell
Basket and Stellate Cells are
Inhibitory in Nature
Get there connection from Mossy Fibers
Cerebellar Output is from
Purkinge cells---> project to the deep nuclei, inhibitory, GABA used
What is the only cell in the cerebellar cortex that is not inhibitory
Granule Cell
Deep Nuclear cells make ___ contacts wherever they project
If one purkinje cell is excited then the other one next to it is also excited or inhibited
What is Dysmetria and what is it a sign of?
overshoots and past pointing
Cerebellar lesions
What is Dysdiadokokinesis
inability to perform rapidly alternating movements such as supination and pronation of hand
Cerebellar lesion
What factor would show that Cerebellum is not to blame?
Paralysis, Rigidity, Obvious Dyskinesias, Deficit in Concious Sensation, Reduction in Muscle strenght
Differentiating drunken gaits:
Cerebellar: not made worse when eyes closed
Dorsal Column Disease: Worse when eyes closed (Romberg)
How is the flocculo-nodular lobe different from the rest of the cerebellum
Receives direct projections from Scarpa's Ganglion (which haven't synapsed in medullary vestibular nuclei)
Some cells project directly to Vestibular nuclei without relying in deep cerebellar nuclei
Lesion in anterior horn cells
Strength: Decreased diffusely,
DTR: Decreased diffusely,
Sensory: Normal
Cranial Nerves: Motor Affected
Root/Plexus Lesion
Strength: Decreased regionally,
DTR: Decreased regionally,
Sensory: Decreased regionally
Cranial Nerves: Normal
Nerve Fiber Lesion
Strength: Decreased Distally,
DTR: Decreased distally,
Sensory: Decrease Distally
Cranial Nerves: Affected if Severe
Neuromuscular junction lesion
Strength: Decreased diffusely,
DTR: Decreased diffusely,
Sensory: Normal
Cranial Nerves: Motor Affected
Muscle Nerve Lesion
Strength: Decreased proximally,
DTR: Decreased proximally
Sensory: Normal
Cranial Nerves: Normal
Perineurium, Endoneurium, Epinerium
Endo- Fiber
Peri - Fasicle
Epi - Nerve
Retrograde Axoplasmic transport uses
Dynein, periphery to cell body
Anterograde Axoplasmic transport
Kinesin, cell body to synapse
When do we observe fiber type grouping?
Deinnervation leads to fiber type grouping instead of random distribution
amyotropic lateral schlerosis
upper and lower motor neuron loss;
no sensory loss; 40% get dementia, survival = 3yrs
Treatment = Rilazole
Loss of Lower motor neuron function, hereditary
spinal muscular atrophy
Polio does what?
Loss of lower motor neuron
Kennedy syndrome
androgen receptor gene;
loss of anterior horn cells in upper cord and brainstem
Anterior and Lower Limb dermatomes
Foot dermatomes
L4,5; S1
Posterior and out limb dermatomes
S1,2, and L5
Radiopathy is a sign of what type of lesion
Root/Plexus: Impingement from herniated nucleus pulposas
abnormal single nerves
Stage1: Neuroprazia ---> dymyelination
Stage 2: Axonotimesis: axonal disruption
Stage 3: Neurotimesis: complete nerve disruption
Mononeuropathy multiplex
Several separate nerves abnormal
all nerves affected the same
Injuries to nerves can affect?
Myelin or the nerve itself.
What is wallerian degeneration
Axon death in 3-8 days
Peripheral axons regrow 1mm/day
If basal membrane and axon are disrupted then the prognosis is?
Causes of mononeuropathy
lyme disease
compression (carpel tunnel)
infarction (diabetes, vasuclitis)
invasion: amyloidosis (abnormal proteins)
Signs of polyneuropathy
Treatment for Guillen Barre
most have full recovery
AcH receptors have what subunits?
2 alpha (where ligand sites are located)
1 beta
1 delta,
1 gamma subunit
What proteins are involved with AcH vesicles attaching to the membrane? What disorders are associated with this
BOTULUSM (irreversibly binds to these proteins)
What is a safety factor
Produce EPP that is 4x that needed to cause an AP to compensate for reduction in Ach. If saftey factor < 1, you see weakness
Myasthenia Gravis pathology and symptoms
Fatigable weakness
Autoimmune attack on receptors
Decreases safety level below threshold
Lambert-Eaton Myathenic Syndrome
autoimmune attack on presynaptic Ca++ channel at active zone leading to impaired vesible reslease and exercise facilitated AcH release
signs of lesions at level of muscle
Proximal>distal weakness, cramps, contracture, atrophy, rhabdoyolysis (muscle fibers into blood stream)
Muscular Dystrophy: Duchennes
Loss of dystrophin (x chromosome), largest gene in body;
Part of dytrophin-glycoprotein complex, which anchors ECM to Merosin, makes sure that the contraction of myofribrils doesn't destroy membrane
How is Becker's different from Duchene's?
Becker has defective but not missing dystrophin
Congenital dystrophies
Problems with anchoring proteins that connect muscle fiber to ECM
Signs of Duchennes
Onset before 5
Wadding gait
Calf Hypertrophy
Severe scholiosis
what is alzheimers of muslce?
Inclusion body myositis, deposition of Amyeloid B into muscle; Most common muscle disorder in patients over 50
Central Cord Syndrome
Arm>leg weakness; Hands especially affected,
variable sensory loss
detrusor hyperflexia
cauda equina syndrome
motor: flaccid paralysis
sensory: saddle anethesia
refexes: hyporefleia
autonomic: overflow incontinence
cauda equina vs medullaris - differences.
urinary retention late = equina
urinary retention early = medullaris
herniation of cerebellar tonsils
- cape like dissociated sensory loss of pain and temp
intact dorsal columns
-hand weakness and atrophy
right parietal lobe is responsible for?
spatial recognition
primary somatosensory, sensory association area
Temporal lobe contains
Primary and secondary associative auditory comple
Wernicke's area
Limbic system medially: emotions, behavior, memory
Corona radiata
Motor sensory perception between cortex and internal capsule
Huntingtons affects what?
Cerebellar Hemispheres are in charge of what?
Limbs, ipsilateral
Cerebellar Vermis Trunks is responsible for what?
UMN weakness below leshion
Pain and temp loss below lesion
LMN weakness at level of lesion
bowel and bladder impairment
Normal posterior column functioning
Anterior cord sydrome
mixed upper and lower deficits:
At level of injury, LMN weakness
UMN weakness below lesion if big
suspended sensory level
Sphincter function preserved
Progressive: Neck--->arm---> leg as lesion expands
Central cord sydrom
Ipsilateral paralysis and loss of vibration/position
contralateral loss of pain and temp
Brown Sequard syndrome
What are the four cardinal signs of parkinsons
Tremor at Rest
Gait, posture, and balance dysfunction
What are the pathological criteria for parkinsons
Lewy bodies
loss of pigmented midbrain cells on substantia nigra
Treatment for parkinsons
Dopamine agonists such as Bromocriptine, Pramipexole, ropinerole
Huntington's Triad
Behavioral Changes
Huntington's pathology
Too much dopamine, autosomal dominant, 100% penetrance, polyglutamate excess
Onset inversely proportional to the number of repeats
anticipation in affected males
Hippocampus: Role and blood flow
short term memory formation
spatial memory and orientation
attention and regulation of mood
Posterior and middle cerebral artery
In hippocampus, what side controls spatial memory and which controls verbal memory
Right - spatial
Left - verbal
activity of hippocampus is modulated by:
estrogen and adrenal steroids
Entorhinal complex degenerates in what syndrome?
Amnesia, confusion, and confabulation in alcoholics is caused by?
Thiamine deficiency ---> necrosis of mammilary bodies

called Wernicke-Korsakoff Syndrome
Infarct of the perforating arteries of the posterior cerebral artery in the anterior nucleus of the thalamus causes?
Role of anterior cingulate gyrus
attention, drive, motivation, initiation of speech
Lesion of anterior cingulate gyrus
Cognitive belt, aka the archicortical circuit
Hippocampus, fornix, mammillary bodies, anterior nucl. of the thalamus, anterior cingulate gyrus, cingulum bundle, hippocampus
Paleocortical division
processing of emotional stimuli
Amygdala, olfactory, orbitofrontal
Amygdala role
input from visual and other sensory modalities,
valence center: attaches affective color or social meaning to sensory info
receives olfactory afferent from olfactory stria
--Startle reflex
--Generation of fight or flight responce
---regulates appetite, mood, agression, and sexual behavior, social behavior, social cues
Connections of amygdala
orbitofrontal cortex
basal forebrain cholinergic receptors in septal nuclei via stria terminalis
hypothalmic and brainstem autonomic areas via ventral amygdalofugal pathways
nucleus accumbens in ventral striatum via extended amygdala
what is the first sign of amygdala seizure
Lesion of the amygdala produces
Kluver-Bucy sydnrome
Hyperorality, hypersexuality, disinhibited behavior
Where are emotional memories made?
If you stimulate the lateral hypothalamic area, you get
agressive, voracious
If you stimulate the ventromedial nucleus, you get
Placid, easy satiety
Lightheadedness is
dysequilibrium is
gait imbalance
Think: cerebellar dysfunciton (gait or truncal ataxia);
sensory dsyfunction ( Rhomberge sign)
extrapyrimidal (pull teste)
decreased visual input, mild or resolving vertigo
Central or peripheral vertigo?
accompanying findings
not as severe
nystagmus that is unilater or bilateral direction shifting with vertical components and cannot be suppressed with fixation of vision
Central or Peripheral vertigo:
in isolation without hearing loss/tinitis
severe, vomiting
nystagmus is always unilateral and suppresible with visual fixation, without vertical components
caloric testing:
warm is ?
cold is ?
warm = stimulatory
cold = inhibitory
difference between labyrinthitis and neuronitis
they are nerve dysfunctions, caused by infection or inflammation.
in vestibular there is no hearing loss while labyrinthitis there is hearing loss...needs antibiotics
If there are bilateral Cerebello-pontine angle tumors it is from
neurofibromatosis II
sudden onset vertigo with a short latency period, worse lying on affective side
BPPV, very common, otolitic debris in semicircular canals
Diagnosis of BPPV?
Treatments for BPPV?
Dix-Hall Pike Maneuver
Epley Maneuver
Medications: Antihistamines, anticholinergics,a dn Benzos
What can cause bilateral peripheral vestibular dysfunction?
aminoglycoside antibiotics (streptomycin, gentamycin)
acute cerebellar strokes and bleeds can lead to?
Primary motor cortex:
SI, Premotor cortex, VL thalamus
internal capsule
pyramindal neurons
Motor cortex lesion
flaccid hemiparesis/hemiplagia on contralateral side initially and later you get spastic
Premotor cortex
Assists with the intergration of sensory and motor information for the performance of an action
Inputs: secondary somatosensory area, ventral anterior thalamic nucleus
Outputs: MI, Contralateral premotor area
Neurons: interneurons
Premotor cortex lesion
contralateral fine motor deficits
difficulty with sensory feedback---control and performance of movements
Frontal Eye Fields

control of voluntary eye movements in the contralateral visual field for processes like active visual search
Intermediate neurons
Frontal eye field lesion
deficits in voluntary visual movement to contralateral visual field
poor visual search
Passive movement is preserved
function: executive processes such as multinodal sensory integration, generation of multiple response alternatives, selection of appropriate response, maintenance of set, persistance, set shifting and flexibility, spatial working memory
Input: thalamus
Outputs: caudate nucleus
Dorsolateral lesion
difficulty integrating sensory nfo
generation of a few stereotyped response alternative
poor judgement
Dorsolateral dysfunction tests
figural fluency (perseveration, alternative responses)
Luria alternating figures test (perseveration, impersistance, appropriate responses)
Copy/free recall (poor organization of learning and recall)
Orbitofrontal cortex
modulation of affective social behavior, working memory for feature information, smell descrimination
INputs: limbic system --> amygdala; olfactory system; inferotemporal lobe (memory formation; ventral visual pathways (form and color)
Output: autonomic musculature, Basal forebrain cholinergic system
orbitofrontal dysfunction
disinhibition and socially inappropriate behavior
failure of feature working memory tasks
Amnosmia (cant smell)
Orbitofrontal tests
Drawing of figures (disinhibition, intrusion)
Go/No-go test (inhibitory behavior)
Cingulate Cortex/Supp Motor Area
Cingulate -(granular)
SMA (Intermediate)
Drive and motivation, environmental exploration
Input/output to deep limbic structures (i.e. nucleus accumbens)
Cingulate Cortex/SMA dysfunction
apathy, akinetic mutism (cingulate)
attentional deficits
delayed habituation to ext. stimuli
Alien Hand syndrome (SMA) --loses control of hand
Frontal-subcortical pathway
frontal cortex-->striatum --> GP/SN--->Thalamus ---> Frontal Cortex
orbitofronal lesion
cingulate gyrus
executive function deficits
Language deficits or emotional processing problems
temporal lobe
Schizophrenia is caused by what
decrease neuronal activeity in dorsolateral prefrontal:subcortical circuits, mediated by dopamine
overactivity in frontal:subcorticol circuits causes
Gegenhalten dystonia
lead pipe resistance different from cogwheeling...frontal lobe
magnetic gait
frontal lobe