What is the main organization pricipal of lower motoneurons?
Organized by movements (direction and force)
What is the main organization principal of upper motoneurons?
Organized on the basis of muscles (innervation destiny and function)
What is one of the major cortical locations of upper motoneurons?
Are motoneurons in the precentral gyrus the only source of corticospinal neurons?
No! only 1/3 from precentral gyrus
Where are Betz cells located?
Primary motor cortex (precentral gyrus) - cross in midline of medulla to innervate anterior horn neurons
The motor cortex is organized into columns of cells with similar actions. What are those actions?
Evoke movement in the same direction
What is the major cause of upper motoneuron lesions?
Cerebrovascular Accident (CVA) involving motor and premotor cortex or internal capsule
What is the cause of hyperreflexia following upper motoneuron lesions?
Return and pathological increase of muscle tone and reflexes after CVA
What accounts for the fact that an upper motoneuron lesion involving the facial nerve leaves the individual with a defect in their ability to smile symmetrically while they are still able to bilaterally move their forehead?
Lower facial muscles innervated by contralateral cortex ONLY; upper face muscles are bilaterally innervated
Name two cortical regions besides the precentral gyrus that contribute axons to the corticospinal tract
Frontal motor cortex
What is the role of the basal ganglia in controlling movement?
Facilitate ongoing movements
Why is dopamine important in movement control?
Essential for normal movements and regulatory control through basal ganglia
Identify the basal ganglia nucleus that contains dopamine containing neurons
Name the major nuclei that comprise the basal ganglia:
What is the return pathway for basal ganglia activity to affect cortically-induced movements?
Name the brain site and the primary lesion in Parkinson's disease
Disinhibition/excitation of the substantia nigra
What role does disinhibition play in mediating actions of the basal ganglia?
Disinhibiton is a reduction of inhibition (GABA) on thalamus that results in excitation of the cerebral cortex
What are the characteristics of Huntingdon's Disease and what region of the brain is involved?
Degeneration in striatum
Hyperkinesia (spontaneous movements)
Dementia and personality disorders
Chorea (continuous movements of face, tongue, or limbs - appear coordinated)
Athetosis (slow, writing movements of hands/fingers)
Hemiballismus (wild, flailing movements of one arm and leg)
How does the cerebellum get information from the motor cortex?
Describe the 2 loops through the cerebellum that relate to motor control
Loop 1: Planning and Execution - wide regions of cerebral cortex make connections through pons to lateral cerebellar hemispheres. (Dentate nucleus --> thalamus --> motor cortex --> activate movement) Dentate neurons fire before onset of movement.
Loop 2: Refine ongoing movement - activation --> intermediate zone (cerebellar cortex) --> interposed nucleus --> red nucleus (spinal cord) --> motor cortex. Primary motor cortex is origin of this component
In which phase of a movement control does the dentate nucelus participate?
Planning and execution
What are the two connections into the Purkinje cells of the cerebellar cortex?
What is the main pathway through which cerebellar information gets back to regions of the motor cortex?
Name a single pathological condition of the cerebellum and describe a few of the symptoms
Changes in emotions - neutral affect - loss of emotions (loss of amygdala)
Hypersexuality - loss of pathways from hypothalamus
Visual agnosia - inability to discriminate visual stimuli (loss of pathways from occipital lobe)
Due to damage of temporal lobe and amygdala (encephalitis, stroke)
Loss of memory
Mood disorder - anxiety depression
Complete loss of cognitive function
Due to neurodegeneration that includes limbic structures
Tx: Aricept - blocks AChase activity - increased ACh
Gall bladder contraction
Increased pyloric constriction (holds nutrients in stomach)
Decreased gastric contractions
Made by stomach
Increased by fasting
Prader Willi Syndrome
Deletion on chromosome 15
Decreased muscle tone
Increased ghrelin secretion
From OB gene
Released by adipocytes
Decreases food intake
Site of action is hypothalamus
Hypothalmic nuclei involved in control of food intake
Lateral hypothalamic area (LHA): activation increases food intake
Paraventricular nucleus (PVN): send axons to brainstem to decrease food intake
Arcuate nucleus (ARC): NPY projects to PVN and LHA and increases food intake (inhibited by leptin); Melanocortin project to PVN and LHA, decreases food intake, stimulated by leptin -- overall leptin effect is to decrease food intake
Loss of vasopressin (ADH) secretion due to head trauma, autoimmune disorder, or idiopathic
Galactorrhea, ameorrhea, hyperprolactinemia
Inappropriate lactation; cessation of menstruation
Due to increased prolactin secretion
Causes decrease in FSH/LH
Usually from micro-adenoma
Remove tumor or tx with DA receptor agonist --> decreased prolactin secretion
Hypothalamic releasing factors
For anterior pituitary
Synthesized in parvocellular neuronsTransported via axons to median eminence