unit 3b Flashcards
Movement disorders
Posterior parietal cortex (PPC)
located posterior to sensorimotor cortex
-Integrates sensory & motor portions of the brain
- processes position of body & objects in space
-controls eye mvmts
Lesions: Problems w/ visual-spatial coordination. problems w/ attention, neglect syndromes
Premotor cortex (PMA)
Located anterior to M1 & inferior to SMA
-Controls postural/trunk & lrg limb muscles
-planning of actions based on sensory cues
-refinement of mvmts based on sensory input w/ cerebellum
Lesions: disruption of learned responses to visual cues
Supplementary Motor area (SMA)
located just anterior to M1 & superior to PMA
-involved in planning learned sequences of mvmts
-activity prior to mvmt
- strong connections w/ subcortical structures
Unilateral Lesions:
~disruption of learned sequence of mvmt
Bilateral lesions:
-blocks all mvmt.
Stimulation:
-creates strong urge to move
Primary motor cortex (M1)
Strip of cortex just anterior to central sulcus (in frontal lobes) where primary control of motor mvmt occurs
M1 contains a body-based motor map similar to somatotopic representation in S1
M1 controls execution of mvmt
Lesions: spastic paralysis
Stimulation: executes a mvmt
Corticospinal (C.S.) tract
the fiber that connect motor cortex thru spinal cord to motor neurons thru-out body
split into 2: Lateral & anterior
Lateral corticospinal tract
80% of the C.S axons cross to other side
- generally go to limbs
Anterior corticospinal tract
20% of C.S. axons DONT cross
- generally go to the trunk
Upper motor neurons
originate in the M1 motor region of the cerebral cortex & carry motor info down to specific spinal cord lvl
the cell bodies of upper motor neurons are in M1 & their axons make up the C.S. tract
Damage: (to cell bodies in M1 or axons along spinal cord) ‘function goes up’ b/c rest of cortex sends inhibitory signal s to lower motor neurons
When a mvmt is made, upper motor neurons stop inhibitory signals to allow lower motor neurons to fire & produce a mvmt
W/ damage to upper motor neurons, baseline inhibitory inputs f/ cortex is lost & lower motor neurons are hyper-active, causing spastic muscles
Lower motor neurons
Bring nerve impulses f/ upper motor neurons out to the muscles
Cell bodies are in spinal cord & send axons to innervate sets of muscles fibers
When damaged : ‘function goes down’
When they dont work, there is no way to send signal to muscles to tell them to contract
- muscles are flaccid (loose + floppy) & eventually atrophy due to loss of neurotrophic (feeding) factors that lower motor neurons also deliver to muscles fibers
Somatotopic organization
organization that follows a map of the body
- ex: neighboring body parts have neighboring representations in cortex
Hemiplegia
total paralysis of arm, leg, & trunk on the same side of body
-usually from lesions to M1
Hemiparesis
weakness on 1 side of the body
Anosognosia
a disorder where the patient is unaware & denies their disability
- often assoc. w/ paralysis & right dorsal parietal damage (also seen in Anton’s syndrome, eating disorders)
Patients typically use confabulations to ‘explain’ why they have the symptoms
Confabulation
Lying unintentionally
A disturbance of memory, defined as production of fabricated, distorted, or misinterpreted memories abt oneself or world, w/o conscious intention to deceive
Certain types of damage to parietal lobes can cause neglect syndromes that are assoc. w/ confabulation
The patient has anosognosia- thus is not aware that they have a deficit (ex: paralysis) & instead come up w/ random/untrue reasons for why they dont have an issue
Anton’s syndrome
blindness & anosognosia f/ dorsal occipital damage
Hemispatial neglect
syndrome where patients are unaware of world/themselves/objects/ visual scene/etc on 1 side of space
- usually the left side f/ damage to right posterior parietal cortex
Gerstmann’s syndrome
syndrome where patients have finger agnosia (can’t identify what their fingers are)
problems w/ left/right differentiation & calculation & writing
Usually cause by damage to inferior part of dominant parietal cortex or can be developmental
Apraxia
disorder of motor planning involving loss of ability to carry out learned purposeful mvmts, despite having desire & physical ability to perform the mvmts
Several sub-types: [Verbal apraxia-apraxia of speech in childhood]
Basal Ganglia
gap of cell bodies below cortex interconnected w/ cortex, thalamus, & brainstem
- involved in motor control * cognition, emotions, + learning
Circuitry includes ‘direct’/excitatory & ‘indirect’/inhibitory pathways
Dopamine
neurotransmitter that plays key role in basal ganglia motor circuit + inhibitory & exhibitory pathways
- also key neurotrans. in arousal + reward syst.
Hypokinetic
characterized by DECREASED mvmt
Hyperkinetic
characterized by INCREASED mvmt
Parkinsons’s disease
A hypo kinetic disease characterized by
- slowing or loss of mvmt (akinesia)
- muscle rigidity
-‘pill-rolling’ tremor at rest
Cause:
- due to loss of dopamine neurons in basal ganglia that cause decrease in activity in basal ganglia’s excitatory ‘direct pathway
Treatments:
- medication (L-Dopa), fetal neural tissue graft, deep brain stimulation (DBS)
Huntington’s chorea
a hyperkinetic disease characterized by:
Cause: autosomal dominant genetic mutation that causes proteins to build up in & ultimately. kill cortical neurons (esp in the inhibitory ‘indirect’ pathway of basal ganglia)
- Cell death is progressive & causes a decline in mental abilities [personality changes, memory issues, dementia] & uncoordinated jerky mvmts (chorea) → eventually leads to death {usually f/ malnutrition due to constant mvmt & or other complications}
Hemiballismus
Relatively rare hyperkinetic disorder characterized by involuntary flinging motions of the extremities - that incr. w/ increased activity
- Symptoms stop during sleep
Causes:
Damage to inhibitory pathway of the motor loop, esp. f/ damage to sub-thalamic nucleus
Treatments: deep brain stimulation, surgery to remove more basal ganglia, drugs that reduce neural signaling
