General overview of somatotropic organization in the sensory and motor homonculus
Face is most lateral, leg/foot is most medial, arm is in the middle of the two
Sensory pathways
-Spinothalamic: pain + temperature
-Dorsal column/medial lemniscus: vibration + propioception
-Trigeminal nerve (CN V): pain, temperature, and touch in the face
Pathway of the spinothalamic tract
3 neurons involved:
1st neuron: brings sensory info to the spinal cord, synapses on 2nd neuron
2nd neuron: decussates in the spinal cord then ascends to the thalamus and synapses on the 3rd neuron
3rd neuron: goes from the thalamus to the sensory cortex
Lesions in the spinothalamic tract (spinal cord vs brainstem/brain)
-Spinal cord (before decussation): ipsilateral loss of pain + temperature sensation
-Brainstem/brain: contralateral loss of pain and temperature sensation
Pathway of the dorsal column/medial lemniscus
3 neurons involved:
1st neuron: enters the spinal cord and ascends to the medulla, synapses on the 2nd neuron in the nucleus gracilis (lower limbs/trunk, below T6) or the nucleus cuneatus (upper limbs/trunk, above T6)
2nd neuron: decussates at the synapse in the medulla, ascends to the thalamus, and synapses on the 3rd neuron
3rd neuron: goes from the thalamus to the sensory cortex
-From the legs (gracilis) goes to the medial sensory cortex
-Info from arms (cuneatus) goes to the lateral sensory cortex
Lesions in the dorsal column/medial lemniscus
-Below the medulla (dorsal column): ipsilateral loss of vibration and proprioception sensation
-Above the medulla (medial lemniscus): contralateral loss of vibration and proprioception sensation
Nerves of the spinothalamic tract vs DC/ML
Spinothalamic tract: small, unmyelinated
DC/ML: small, unmyelinated
Visual pathway (7)
Retina –> optic nerve –> optic chiasm –> optic tract –> thalamus (lateral geniculate nucleus) –> optic radiations (white matter tracts) –> primary visual cortex
Optic nerve lesion
Total loss of vision in the affected eye
Heteronymous hemianopsia
-Lesion in the optic chiasm
-Loss of vision of both lateral visual fields (input from medial retina)
Homonymous hemianopsia
-Lesion in the optic tract
-Lose vision in either the left or right visual fields in both eyes (input from one medial retina and one lateral retina)
Quadrantanopia
Loss of vision in either the upper left or right quadrants of the visual field in both eyes
Caused by temporal lobe - optic radiation tract (Meyer’s loop) lesion
Lesions in the other sensory systems (hearing, taste, smell)
These systems have bilateral representation in the brain, so unilateral cortical lesions don’t cause loss of hearing, taste, or smell
Two general systems of motor pathways
Pyramidal: direct motor pathways, control voluntary, precise movements
-Corticospinal tract
Extrapyramidal: indirect motor pathways, modulation + coordination of movement (posture, tone, balance, autonomic/habitual movements)
-Basal ganglia
-Cerebellum
Basal ganglia communication pathway in the brain
Cortico-BG-thalamo-cortico loop:
cortex –> BG –> thalamus –> cortex
Two examples of lesions in the basal ganglia
-Lesion in the substantia nigra = Parkinson’s
-Lesion in the caudate nucleus = Huntington’s
Function of the cerebellum
Precise, coordinated movement
Ex: finger to nose coordination - smooth, direct line movements
What are the inputs to the cerebellum? (3)
-Cerebral cortex (cortical input)
-Vestibular system (vestibular input)
-Spinal cord (spinal input)
Pathway of cerebellar output
Cerebellum –> contralateral thalamus –> ipsilateral motor cortex –> corticospinal tract
*The cerebellar output decussates twice (the corticospinal tract decussates in the medulla), which means that output ultimately affects the ipsilateral side of the body
Lesions in the cerebellum cause what?
Ipsilateral ataxia - impaired coordination of voluntary muscle movement
Corticospinal tract overview
Efferent (descending) pathway - motor control of skeletal muscles (voluntary movement)
Corticospinal tract pathway
UMN: primary motor cortex –> internal capsule –> midbrain –> pons –> medulla (pyramidal decussation) –> LMN (in the spinal cord)
*The LMN is NOT part of the tract. It goes from the spinal cord –> skeletal muscle
Lesions of the corticospinal tract (UMNs) cause what? (3?)
-Weakness (of affected region)
-Hyperreflexia
-Spasticity
Why do UMN lesions cause hyperreflexia and spasiticy?
Because the UMNs normally send inhibitory signals down to spinal reflex circuits, keeping muscle tone + reflexes under control.
When there’s a lesion, inhibitory control is lost, and the LMNs and reflex arcs in the spinal cord become overactive.
Results:
-Even minor sensory inputs can trigger exaggerated reflexes
-Increased muscle tone (spasticity) - muscles resist being stretched because of stretch reflex being active