5.1 Sensory Receptors, Somatic Sensation, Spinal Reflexes & Motor Control
Key Takeaways
Fine touch, vibration and proprioception ascend in the dorsal columns and cross in the medulla; pain and temperature cross within one or two cord segments and ascend in the spinothalamic tract.
The muscle spindle (Ia afferent) drives the monosynaptic stretch reflex; the Golgi tendon organ (Ib afferent) senses tension and inhibits its own muscle.
Upper motor neuron lesions cause spasticity, hyperreflexia and an extensor plantar (Babinski) response; lower motor neuron lesions cause flaccid weakness, atrophy, fasciculations and areflexia.
Cerebellar hemisphere lesions cause ipsilateral dysmetria, intention tremor and dysdiadochokinesia; vermis lesions cause truncal ataxia.
Parkinson disease follows loss of dopaminergic neurons in the substantia nigra pars compacta; Huntington disease follows loss of striatal GABA neurons; subthalamic lesions cause contralateral hemiballismus.
Why this area matters
The TOS neurophysiology list continues after action potentials with:
- motor functions of the spinal cord and cord reflexes;
- muscle sensory receptors;
- cortical and brainstem control of motor function;
- the cerebellum, basal ganglia and overall motor control;
- somatic sensations.
The same localizing logic is used in Anatomy, Medicine (stroke, neuropathy) and Surgery (spinal cord injury).
Sensory receptors and fibers
Receptors convert a stimulus into a graded receptor potential, and stronger stimuli produce higher firing frequencies.
- Rapidly adapting receptors signal change. Pacinian corpuscles sense vibration, and Meissner corpuscles sense light touch.
- Slowly adapting receptors signal sustained stimuli: Merkel discs (pressure), Ruffini endings (stretch), muscle spindles and nociceptors.
| Fiber | Diameter and myelin | Carries |
|---|---|---|
| A-alpha (Ia, Ib) | Largest, myelinated | Muscle spindle and Golgi tendon organ afferents |
| A-beta | Large, myelinated | Touch, pressure, vibration |
| A-delta | Small, thinly myelinated | Sharp, fast pain; cold |
| C | Smallest, unmyelinated | Dull, slow, burning pain; warmth; itch |
Pain modulation:
- In the gate control model, A-beta touch input inhibits pain transmission in the dorsal horn, which is why rubbing an injury helps.
- Descending inhibition from the periaqueductal gray and the nucleus raphe magnus uses endogenous opioids, serotonin and norepinephrine.
- Referred pain occurs because visceral and somatic afferents converge on the same dorsal horn neurons. Examples: cardiac pain felt in the left arm, diaphragmatic irritation in the shoulder, early appendicitis around the umbilicus.
Somatic sensory pathways
| Pathway | Modalities | Where it crosses | Course |
|---|---|---|---|
| Dorsal column-medial lemniscus | Fine touch, vibration, conscious proprioception | Medulla (internal arcuate fibers) | Gracilis (leg) and cuneatus (arm), then the medial lemniscus, then the VPL thalamus, then the postcentral gyrus |
| Anterolateral (spinothalamic) | Pain, temperature, crude touch | Spinal cord, within 1 or 2 segments via the anterior white commissure | Contralateral spinothalamic tract, then the VPL thalamus, then the postcentral gyrus |
Brown-Séquard syndrome (cord hemisection) produces, below the lesion:
- ipsilateral weakness and upper motor neuron signs;
- ipsilateral loss of vibration and proprioception;
- contralateral loss of pain and temperature.
Central cord syndrome (syringomyelia, hyperextension injury) produces cape-like loss of pain and temperature with weakness of the arms more than the legs.
Spinal cord reflexes
- Stretch (myotatic) reflex. Stretching a muscle stretches its spindles (intrafusal fibers). Ia afferents excite the alpha motor neurons of the same muscle monosynaptically and inhibit the antagonist through an interneuron (reciprocal inhibition). Gamma motor neurons keep the spindle sensitive while the muscle shortens.
- Golgi tendon organ. It lies in series with the muscle at the tendon, senses tension, and through Ib afferents and inhibitory interneurons relaxes the same muscle (autogenic inhibition). This protects against excessive force and underlies the clasp-knife phenomenon.
- Flexor withdrawal and crossed extensor reflex. A painful stimulus causes withdrawal of the limb and extension of the opposite limb to support body weight. The reflex is polysynaptic.
| Deep tendon reflex | Root level |
|---|---|
| Biceps, brachioradialis | C5, C6 |
| Triceps | C7 (C6 to C8) |
| Patellar (knee) | L3, L4 |
| Achilles (ankle) | S1 |
Upper versus lower motor neuron lesions
| Sign | Upper motor neuron (cortex, internal capsule, corticospinal tract) | Lower motor neuron (anterior horn cell, root, nerve) |
|---|---|---|
| Tone | Increased (spastic, velocity-dependent) | Decreased (flaccid) |
| Reflexes | Brisk, with clonus | Reduced or absent |
| Plantar response | Extensor (Babinski sign) | Flexor or absent |
| Bulk | Mild disuse atrophy | Marked atrophy |
| Fasciculations | Absent | Present |
Amyotrophic lateral sclerosis shows both sets of signs. Acute spinal cord injury causes spinal shock at first: flaccidity and areflexia below the level, followed after days to weeks by spasticity and hyperreflexia.
Cortical and brainstem control of movement
- The primary motor cortex (precentral gyrus) is arranged as a homunculus. The face and arm are on the lateral surface (middle cerebral artery territory) and the leg is on the medial surface (anterior cerebral artery territory).
- The premotor and supplementary motor areas plan sequences of movement.
- Most corticospinal fibers (about 80% to 90%) cross at the pyramidal decussation in the lower medulla and descend in the lateral corticospinal tract. A lesion above the decussation therefore causes contralateral weakness.
- Brainstem pathways:
- Vestibulospinal and pontine reticulospinal tracts excite antigravity extensors.
- The rubrospinal tract favors upper-limb flexion.
- Decorticate posturing (flexed arms, extended legs) indicates a lesion above the red nucleus.
- Decerebrate posturing (extended arms and legs) indicates a lesion between the red and vestibular nuclei and carries a worse prognosis.
The cerebellum
The cerebellum compares the intended movement with sensory feedback and corrects errors. It works through feed-forward timing and does not start movements.
- Vermis and flocculonodular lobe lesions cause truncal ataxia, a wide-based gait and nystagmus. Alcoholic degeneration affects the anterior vermis.
- Hemisphere lesions cause signs on the same side: dysmetria (past-pointing), intention tremor, dysdiadochokinesia, rebound and hypotonia.
The basal ganglia
The striatum (caudate and putamen) receives cortical input and sends output through the globus pallidus internus and substantia nigra pars reticulata to the thalamus.
- In the direct pathway (D1 receptors), dopamine increases thalamocortical drive and facilitates movement.
- In the indirect pathway (D2 receptors, via the subthalamic nucleus), dopamine reduces the pathway's braking effect, so movement is also facilitated.
| Disorder | Lesion | Result |
|---|---|---|
| Parkinson disease | Loss of dopaminergic neurons in the substantia nigra pars compacta (Lewy bodies) | Bradykinesia, cogwheel rigidity, resting pill-rolling tremor, shuffling gait |
| Huntington disease | Loss of striatal GABA neurons (caudate atrophy), autosomal dominant CAG repeat | Chorea, dementia, psychiatric change |
| Hemiballismus | Subthalamic nucleus (often a lacunar stroke) | Violent flinging of the contralateral limbs |
A man stabbed in the back has a right-sided spinal cord hemisection at T10. Which neurologic pattern is expected below the lesion?
Left leg weakness and loss of vibration sense, with loss of pain and temperature in the right leg
Loss of all sensation in both legs with preserved motor function
Bilateral leg weakness with preserved sensation in both legs
Right leg weakness and loss of vibration sense, with loss of pain and temperature in the left leg
A patient with a right cerebellar hemisphere metastasis is asked to touch his nose and then the examiner's finger. Which finding is expected?
A resting tremor in the left hand that disappears with movement
Spastic weakness and hyperreflexia of the left arm
An intention tremor and past-pointing in the right arm
Loss of joint-position sense in the left fingers
A 60-year-old has a resting pill-rolling tremor of the right hand, cogwheel rigidity and slow, shuffling gait. Loss of which neurons best explains these signs?
GABAergic neurons of the caudate nucleus
Glutamatergic neurons of the subthalamic nucleus
Purkinje cells of the cerebellar vermis
Dopaminergic neurons of the substantia nigra pars compacta
Sections you finish are checked off in the contents.