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197 Cards in this Set
- Front
- Back
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Hypokinesia
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Decreased body movement
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Bradykinesia
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Slow body movements
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Apraxia
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loss of ability to preform previously learned purposeful motor act in the absence of any overt primary motor or sensory loss
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Akinesia-
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reduced spontaneous movements
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Chorea
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meaning “dance” in Greek, this refers to random, purposeless, jerky movements
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Dystonia
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abnormal postures, usually associated with movements, typically turning in nature, caused by
co-contraction of agonist and antagonist muscles |
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Clonus
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a regular, large amplitude jerk or series of jerks, slower than myoclonus, associated with
spasticity or seizures |
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What muscle is voluntary? Involuntary?
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Striated or Skeletal
Smooth and Cardiac |
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What is the neurotransmitter used with muscles?
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acetylcholine
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What is a high safety factor?
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1:1 relationship between AP in motor axon and contraction of muscle fiber
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Differences between slow and fast muscle
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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) |
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LMN is a _____motor neuron
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Alpha
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Each muscle fiber has innervation from ___ motor neuron, with the exception of _____
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1 motor neuron, extraocular muscles
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What is a motor neuron pool?
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all alpha motor neurons innervating one muscle.
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Difference between fibrillations and fasciculations.
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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 |
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How does the CNS control muscular contraction?
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Number of alpha motor neurons (recruitment of small fibers first)
Firing rates |
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Golgi tendon organ is a _____?
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proprioceptor
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Golgi tendon senses _____ through what type of fiber?
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Force, IB ----> spinal cord
Sensitive to contraction of a small number of motor units Insensitive to passive strethc |
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Muscle spindle senses____? Via what kind of fibers?
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Stretch
Ia (velocity) and II (length) ----> CNS |
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Intrafusal fibers are what? Innervation>
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small fibers of the spindle (Gamma innervation)
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Extrafusal fibers?
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Outside spindle
Alpha motor neurons |
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Two ways to make Ia fire stronger:
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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 |
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How do gamma neurons work?
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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.
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Do intrafusal fibers generate APs? Do they contribute to the force of a muscle
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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 |
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What is alpha-gamma coactivation?
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It when gamma and alpha are activated together such that extra and intrafusal fibers contract and expand together.
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Ia axons are found in what part of the spindle? What do II fibers do?
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equatorial region of intrafusal muscle fiber
II fibers report steady state length of a muscle |
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What is the gamma loop?
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gamma activation --> intrafusal shortening --> Ia activation ---> alpha activation ---> extrafusal contraction
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High gamma motor neuron activity can lead to
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Hypertonia
hyperreflexia: increased sanity of the gamma loop to muscle stretch |
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How does one cure rigidity caused by gamma motor neuron increased firing
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cut dorsal root (where gamma mn enter)
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What is the motor neuron organization in the spinal cord?
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axial and proximal mn are found medially
distal mn are found laterally |
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Describe a monosynaptic reflex
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-Ia and alpha motor neuron on Homonymous muscle.
-Reciprocal innervation (Ia inhibits neurons of antagonist va inhibitory interneuron -segmental sensory and motor function test |
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What is the Hoffman reflex?
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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 |
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What is the Jendrassik's maneuver?
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increases gamma neuron activity via propriospinal pathway. When pulling your hands apart you get larger reflex.
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what happens when you increase load?
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increase stretch, increase firing of Ia afferents, increase firing of motor neurons
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what is spasticity?
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increase in resting motor tone
increase in reflex excitability |
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If you cut the dorsal horn to treat spasticity and it is not successful, what does this indicate?
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Excitability not due to Ia afferent input
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How does the flexor and extensor reflex work
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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. |
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When would you see spontaneous crossed extensor reflex?
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in babies. goes away around 3 months of age.
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What are the three major descending motor pathways?
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1) Ventromedial pathway (tectospinal, vestibulospinal, and reticulospinal).
2) Lateral Brainstem Pathway (rubrospinal) 3) Corticospinal pathway (pyrimidal) |
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What pathway goes through the midbrain tectum? What does it control?
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Tectospinal - Axial muscles
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What pathway goes through the red nucleus
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Lateral brainstem pathway --> rubospinal pathway
Does girdle and proximal upper limb muslces |
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What pathway has its nucleus in the medulla?
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Vestibular and Reticular (medulla + pons)
They both operate on axial muscles |
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What tracts do not decussate?
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reticulospinal and rubrospinal
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Reticular formation has what function?
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keeps you awake!
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What tracts send projections bilaterally?
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vestibulospinal and tectospinal.
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Decorticate rigidity vs decerebrate rigidity
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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 |
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Possible causes of decerebrate rigidity
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syrinx (cystic cavity) around ventricle in the brainstem or central cord of spinal cord
Basilar occlusion |
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Locked in Sydnrome
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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. |
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What is the role of the premotor cortex and supplementary motor cortex
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Area 6 (premotor is lateral and supplementary is medial).
Motor planning. Imagining a movement. |
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What are the inputs to the Motor Cortex?
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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 |
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Outputs of motor cortex
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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) |
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SMA, PMA, or Posterior Parietal Lesions
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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 |
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Neglect syndromes results from what?
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Posterior parietal legions
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Supranuclear lesion of Cranial Nerve VII
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can move forehead but not lower half of face, sign of a stroke
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Upper face is special, why?
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It has dual innervation via corticobulbar tract
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When we are learning a task, we do what
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recruit motor neurons
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What artery supplies the internal capsule
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Internal Carotid
Middle Cerebral |
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Basal ganglia is supplied by what vessel?
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MCA
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Name the parts of the Basal Ganglia
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Caudate
Putamen Globus Palladus (Internal and External) N. Accumbens Substantia Nigra Subthalamic Nucleus |
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Does the Basal Ganglia have a direct connection to the cerebral cortex?
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NO! Output is two the VL nucleus of the thalamus.
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What part of substantia nigra has dopamine cells lost in parkinsons
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pars compacta
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Basal Ganglia Loop is INhibitory or excitatory
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Inhibitory
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Describe the indirect tract in Basal ganglia
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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
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Describe direct loop
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Striatum inhibits Gpi, which decrease inhibition of thalamus which increases activation of cortecx
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What modulates the Basal Ganglia
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Substantia nigra (Dopamine)
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What are the three loops of the Basal Ganglia
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Sensorimotor ---> Putamen (Movement)
Prefrontal ---> Caudate (Memory) Limbic ---> Accumbens (Mood) |
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Dystonia
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Abnormal resting muscle tone
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Dyskinesia
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Involuntary or Abnormal movements
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Basal Ganglia lesion signs
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Dyskinesias (akinesia, bradykinesia, tremor, chorea, athetosis, Ballism, blepharospasm)
Dystonias |
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What is Ballism
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involuntary flinging of the extremities, usually unilateral.
Cause: Less Gpi Excitation, less inhibition of thalamus |
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Cerebellar peduncle paths
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Superior --> Output
Middle---> inputs pontine projections Inferior ---> inputs from inferior olive |
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Outputs of Superior Cerebellar Peduncle
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Fastigial nucleus ---> Vesticular and reticular nuclei
Interpositus nucleus --> Red Nucleus Dentate Nucleus ---> Thalamus (cortex) |
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What is an intention tremor
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nearer to target. Increases on movement
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what is the first sign of midline cerebellar tumors
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truncal ataxia
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lateral lesions of cerebellum affect what?
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Movement of limbs
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Do more axons enter or leave the cerebellum?
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Enter
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Ipsilateral cerebellar hemisphere connects to ___ cerebral hemisphere
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Contralateral
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Which spinal tract does a double decussation
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Rubropsinal tract (R. Interpossitus nucleus--->L. red nucleus ---> Right spinal cord
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How do the cerebllar cortex and deep nuclei interact?
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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 |
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Mossy fibers are:
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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 |
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Climbing fibers
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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 |
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Basket and Stellate Cells are
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Inhibitory in Nature
Get there connection from Mossy Fibers |
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Cerebellar Output is from
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Purkinge cells---> project to the deep nuclei, inhibitory, GABA used
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What is the only cell in the cerebellar cortex that is not inhibitory
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Granule Cell
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Deep Nuclear cells make ___ contacts wherever they project
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excitatory
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If one purkinje cell is excited then the other one next to it is also excited or inhibited
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Inhibited
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What is Dysmetria and what is it a sign of?
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overshoots and past pointing
Cerebellar lesions |
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What is Dysdiadokokinesis
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inability to perform rapidly alternating movements such as supination and pronation of hand
Cerebellar lesion |
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What factor would show that Cerebellum is not to blame?
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Paralysis, Rigidity, Obvious Dyskinesias, Deficit in Concious Sensation, Reduction in Muscle strenght
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Differentiating drunken gaits:
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Cerebellar: not made worse when eyes closed
Dorsal Column Disease: Worse when eyes closed (Romberg) |
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How is the flocculo-nodular lobe different from the rest of the cerebellum
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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 |
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Lesion in anterior horn cells
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Strength: Decreased diffusely,
DTR: Decreased diffusely, Sensory: Normal Cranial Nerves: Motor Affected |
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Root/Plexus Lesion
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Strength: Decreased regionally,
DTR: Decreased regionally, Sensory: Decreased regionally Cranial Nerves: Normal |
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Nerve Fiber Lesion
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Strength: Decreased Distally,
DTR: Decreased distally, Sensory: Decrease Distally Cranial Nerves: Affected if Severe |
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Neuromuscular junction lesion
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Strength: Decreased diffusely,
DTR: Decreased diffusely, Sensory: Normal Cranial Nerves: Motor Affected |
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Muscle Nerve Lesion
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Strength: Decreased proximally,
DTR: Decreased proximally Sensory: Normal Cranial Nerves: Normal |
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Perineurium, Endoneurium, Epinerium
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Endo- Fiber
Peri - Fasicle Epi - Nerve |
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Retrograde Axoplasmic transport uses
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Dynein, periphery to cell body
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Anterograde Axoplasmic transport
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Kinesin, cell body to synapse
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When do we observe fiber type grouping?
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Deinnervation leads to fiber type grouping instead of random distribution
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amyotropic lateral schlerosis
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upper and lower motor neuron loss;
no sensory loss; 40% get dementia, survival = 3yrs Treatment = Rilazole |
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Loss of Lower motor neuron function, hereditary
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spinal muscular atrophy
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Polio does what?
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Loss of lower motor neuron
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Kennedy syndrome
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androgen receptor gene;
loss of anterior horn cells in upper cord and brainstem |
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Anterior and Lower Limb dermatomes
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L1-4
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Foot dermatomes
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L4,5; S1
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Posterior and out limb dermatomes
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S1,2, and L5
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Radiopathy is a sign of what type of lesion
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Root/Plexus: Impingement from herniated nucleus pulposas
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Mononeuropathy;
Stages |
abnormal single nerves
Stage1: Neuroprazia ---> dymyelination Stage 2: Axonotimesis: axonal disruption Stage 3: Neurotimesis: complete nerve disruption |
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Mononeuropathy multiplex
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Several separate nerves abnormal
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Polyneuropathy
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all nerves affected the same
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Injuries to nerves can affect?
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Myelin or the nerve itself.
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What is wallerian degeneration
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Axon death in 3-8 days
Peripheral axons regrow 1mm/day |
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If basal membrane and axon are disrupted then the prognosis is?
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Bad
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Causes of mononeuropathy
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lyme disease
compression (carpel tunnel) trauma infarction (diabetes, vasuclitis) invasion: amyloidosis (abnormal proteins) |
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Signs of polyneuropathy
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Areflexic,
Symmetric |
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Treatment for Guillen Barre
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plasmapharesis
most have full recovery |
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AcH receptors have what subunits?
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2 alpha (where ligand sites are located)
1 beta 1 delta, 1 gamma subunit |
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What proteins are involved with AcH vesicles attaching to the membrane? What disorders are associated with this
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synaptobrevin
SNAP 25 syntaxin BOTULUSM (irreversibly binds to these proteins) |
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What is a safety factor
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Produce EPP that is 4x that needed to cause an AP to compensate for reduction in Ach. If saftey factor < 1, you see weakness
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Myasthenia Gravis pathology and symptoms
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Fatigable weakness
Autoimmune attack on receptors Decreases safety level below threshold POSTSYNAPTIC DISEASE |
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Lambert-Eaton Myathenic Syndrome
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PRESYNAPTIC DISEASE
autoimmune attack on presynaptic Ca++ channel at active zone leading to impaired vesible reslease and exercise facilitated AcH release |
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signs of lesions at level of muscle
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Proximal>distal weakness, cramps, contracture, atrophy, rhabdoyolysis (muscle fibers into blood stream)
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Muscular Dystrophy: Duchennes
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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 |
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How is Becker's different from Duchene's?
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Becker has defective but not missing dystrophin
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Congenital dystrophies
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Problems with anchoring proteins that connect muscle fiber to ECM
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Signs of Duchennes
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Onset before 5
Wadding gait Calf Hypertrophy Cardiac Severe scholiosis |
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what is alzheimers of muslce?
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Inclusion body myositis, deposition of Amyeloid B into muscle; Most common muscle disorder in patients over 50
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Central Cord Syndrome
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Arm>leg weakness; Hands especially affected,
variable sensory loss detrusor hyperflexia |
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cauda equina syndrome
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motor: flaccid paralysis
sensory: saddle anethesia refexes: hyporefleia autonomic: overflow incontinence |
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cauda equina vs medullaris - differences.
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urinary retention late = equina
urinary retention early = medullaris |
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syringomyelia
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herniation of cerebellar tonsils
- cape like dissociated sensory loss of pain and temp intact dorsal columns -hand weakness and atrophy -spasticity |
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right parietal lobe is responsible for?
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spatial recognition
manipulation primary somatosensory, sensory association area |
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Temporal lobe contains
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Primary and secondary associative auditory comple
Wernicke's area Limbic system medially: emotions, behavior, memory |
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Corona radiata
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Motor sensory perception between cortex and internal capsule
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Huntingtons affects what?
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Caudate
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Cerebellar Hemispheres are in charge of what?
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Limbs, ipsilateral
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Cerebellar Vermis Trunks is responsible for what?
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Stance/Gait
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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
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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
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Ipsilateral paralysis and loss of vibration/position
contralateral loss of pain and temp |
Brown Sequard syndrome
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What are the four cardinal signs of parkinsons
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Rigidity
Tremor at Rest Hypokinesia Gait, posture, and balance dysfunction |
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What are the pathological criteria for parkinsons
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Lewy bodies
loss of pigmented midbrain cells on substantia nigra |
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Treatment for parkinsons
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L-Dopa
Dopamine agonists such as Bromocriptine, Pramipexole, ropinerole |
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Huntington's Triad
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Dementia
Chorea Behavioral Changes |
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Huntington's pathology
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Too much dopamine, autosomal dominant, 100% penetrance, polyglutamate excess
Onset inversely proportional to the number of repeats anticipation in affected males |
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Hippocampus: Role and blood flow
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Role:
short term memory formation spatial memory and orientation attention and regulation of mood Posterior and middle cerebral artery |
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In hippocampus, what side controls spatial memory and which controls verbal memory
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Right - spatial
Left - verbal |
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activity of hippocampus is modulated by:
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estrogen and adrenal steroids
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Entorhinal complex degenerates in what syndrome?
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Alzheimers
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Amnesia, confusion, and confabulation in alcoholics is caused by?
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Thiamine deficiency ---> necrosis of mammilary bodies
called Wernicke-Korsakoff Syndrome |
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Infarct of the perforating arteries of the posterior cerebral artery in the anterior nucleus of the thalamus causes?
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Amnesia
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Role of anterior cingulate gyrus
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attention, drive, motivation, initiation of speech
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Lesion of anterior cingulate gyrus
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apathy
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Cognitive belt, aka the archicortical circuit
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Hippocampus, fornix, mammillary bodies, anterior nucl. of the thalamus, anterior cingulate gyrus, cingulum bundle, hippocampus
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Paleocortical division
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processing of emotional stimuli
Amygdala, olfactory, orbitofrontal |
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Amygdala role
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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 |
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Connections of amygdala
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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 |
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what is the first sign of amygdala seizure
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fear
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Lesion of the amygdala produces
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Kluver-Bucy sydnrome
Hyperorality, hypersexuality, disinhibited behavior |
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Where are emotional memories made?
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Amygdala
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If you stimulate the lateral hypothalamic area, you get
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agressive, voracious
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If you stimulate the ventromedial nucleus, you get
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Placid, easy satiety
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Lightheadedness is
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presyncope
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dysequilibrium is
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gait imbalance
Think: cerebellar dysfunciton (gait or truncal ataxia); sensory dsyfunction ( Rhomberge sign) extrapyrimidal (pull teste) decreased visual input, mild or resolving vertigo |
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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
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Central or Peripheral vertigo:
in isolation without hearing loss/tinitis severe, vomiting nystagmus is always unilateral and suppresible with visual fixation, without vertical components |
peripheral
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caloric testing:
warm is ? cold is ? |
warm = stimulatory
cold = inhibitory |
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difference between labyrinthitis and neuronitis
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they are nerve dysfunctions, caused by infection or inflammation.
in vestibular there is no hearing loss while labyrinthitis there is hearing loss...needs antibiotics |
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If there are bilateral Cerebello-pontine angle tumors it is from
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neurofibromatosis II
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sudden onset vertigo with a short latency period, worse lying on affective side
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BPPV, very common, otolitic debris in semicircular canals
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Diagnosis of BPPV?
Treatments for BPPV? |
Dix-Hall Pike Maneuver
Epley Maneuver Medications: Antihistamines, anticholinergics,a dn Benzos |
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What can cause bilateral peripheral vestibular dysfunction?
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aminoglycoside antibiotics (streptomycin, gentamycin)
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acute cerebellar strokes and bleeds can lead to?
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Verigo
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Primary motor cortex:
inputs outputs nuerons |
SI, Premotor cortex, VL thalamus
internal capsule pyramindal neurons |
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Motor cortex lesion
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flaccid hemiparesis/hemiplagia on contralateral side initially and later you get spastic
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Premotor cortex
inputs outputs nuerons |
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 |
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Premotor cortex lesion
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apraxia
contralateral fine motor deficits difficulty with sensory feedback---control and performance of movements |
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Frontal Eye Fields
nuerons |
control of voluntary eye movements in the contralateral visual field for processes like active visual search
Intermediate neurons |
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Frontal eye field lesion
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deficits in voluntary visual movement to contralateral visual field
poor visual search Passive movement is preserved |
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Dorsolateral
inputs outputs nuerons |
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 |
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Dorsolateral lesion
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difficulty integrating sensory nfo
generation of a few stereotyped response alternative poor judgement impersistance perseveration |
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Dorsolateral dysfunction tests
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figural fluency (perseveration, alternative responses)
Luria alternating figures test (perseveration, impersistance, appropriate responses) Copy/free recall (poor organization of learning and recall) |
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Orbitofrontal cortex
inputs outputs nuerons |
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 |
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orbitofrontal dysfunction
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disinhibition and socially inappropriate behavior
failure of feature working memory tasks Amnosmia (cant smell) confabulation |
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Orbitofrontal tests
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Drawing of figures (disinhibition, intrusion)
Go/No-go test (inhibitory behavior) |
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Cingulate Cortex/Supp Motor Area
inputs outputs neurons |
Cingulate -(granular)
SMA (Intermediate) Drive and motivation, environmental exploration Input/output to deep limbic structures (i.e. nucleus accumbens) |
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Cingulate Cortex/SMA dysfunction
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apathy, akinetic mutism (cingulate)
attentional deficits delayed habituation to ext. stimuli Alien Hand syndrome (SMA) --loses control of hand |
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Frontal-subcortical pathway
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frontal cortex-->striatum --> GP/SN--->Thalamus ---> Frontal Cortex
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Disinhibition
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orbitofronal lesion
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apathy
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cingulate gyrus
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executive function deficits
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Dorsolateral
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Language deficits or emotional processing problems
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temporal lobe
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Schizophrenia is caused by what
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decrease neuronal activeity in dorsolateral prefrontal:subcortical circuits, mediated by dopamine
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overactivity in frontal:subcorticol circuits causes
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OCD
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Gegenhalten dystonia
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lead pipe resistance different from cogwheeling...frontal lobe
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magnetic gait
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frontal lobe
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