Speech, motor and sensory systems
Language and speech; motor and sensory systems
Language depends on a left-hemisphere network, speech on the muscles and nerves that shape sound, movement on the corticospinal tract and its lower motor neurones, and sensation on two ascending pathways that cross at different levels. CPSP asks which lesion causes which aphasia or dysarthria, how upper and lower motor neurone signs differ, and where to look on MRI for a sensory or motor deficit.
Language areas and dominance
- Broca area (inferior frontal gyrus, areas 44 and 45): speech production and grammar. Wernicke area (posterior superior temporal gyrus, area 22): comprehension. The arcuate fasciculus links them. The planum temporale, behind Heschl gyrus, is usually larger on the left and serves comprehension.
- Language is in the left hemisphere in almost all right-handers and most left-handers. A large left hemisphere injury at birth lets language develop in the right hemisphere (plasticity), so speech may be normal.
- The right hemisphere carries emotional prosody: a right frontal lesion leaves words and grammar intact but the voice flat (aprosodia).
| Aphasia | Fluency | Comprehension | Repetition | Lesion |
|---|---|---|---|---|
| Broca | Poor | Good | Poor | Inferior frontal gyrus |
| Wernicke | Fluent, often meaningless | Poor | Poor | Posterior superior temporal gyrus |
| Conduction | Fluent | Good | Poor | Arcuate fasciculus |
| Transcortical motor | Poor | Good | Preserved | Frontal, sparing Broca |
| Transcortical sensory | Fluent | Poor | Preserved | Temporoparietal, sparing Wernicke |
| Global | Poor | Poor | Poor | Whole perisylvian region |
Speech production (dysarthria and voice)
| Problem | Cause and mechanism |
|---|---|
| Slow speech split into syllables with uneven loudness (scanning) | Cerebellum and its connections (multiple sclerosis) |
| Nasal speech, choking, wasted fasciculating tongue, absent jaw jerk | Lower motor neurones of the medullary nuclei (bulbar palsy, syringobulbia) |
| Slow spastic speech, brisk jaw jerk | Bilateral corticobulbar (pseudobulbar) lesions |
| Hypernasal speech, air escape on "p" and "b", nasal regurgitation | Failure of velopharyngeal closure by the soft palate (after adenoidectomy) |
| Speech after laryngectomy | Swallowed air vibrates the pharyngo-oesophageal segment |
Motor system
- Corticospinal tract: from motor cortex (area 4 and premotor areas) through the posterior limb of the internal capsule, cerebral peduncle and medullary pyramid; most fibres cross at the decussation to form the lateral corticospinal tract, which is essential for fine, fractionated finger movement. The rest descend uncrossed.
| Sign | Upper motor neurone | Lower motor neurone |
|---|---|---|
| Tone | Spastic | Flaccid |
| Reflexes | Brisk; Hoffmann sign (lesion above C8) | Reduced or absent |
| Plantar | Extensor | Flexor or absent |
| Superficial abdominal reflexes | Lost early (they need corticospinal input) | Lost only if their segments are affected |
| Wasting and fasciculation | Little | Marked |
- An extensor plantar is normal in infants because the corticospinal tracts are not fully myelinated until about the second year.
- Inverted supinator jerk: absent biceps and supinator jerks with finger flexion when the radius is tapped mean a C5–C6 cord lesion (cervical myelopathy).
- Poliomyelitis kills anterior horn cells; survivors sprout collaterals to adopt orphaned fibres, so EMG shows few, very large, long motor units.
- Posture: decerebrate (extensor) posturing follows a lesion between the red nucleus and vestibular nuclei; decorticate (flexed arms) follows a lesion above the red nucleus.
Sensory systems
| Pathway | Carries | Fibres | Crosses |
|---|---|---|---|
| Dorsal column–medial lemniscus | Fine touch, vibration, joint position | Large myelinated | Medulla (internal arcuate fibres) |
| Lateral spinothalamic | Pain and temperature | Aδ (fast) and C (slow) | Within one or two segments, in the anterior white commissure |
- Fast pain (Aδ, neospinothalamic) is sharp and well localised; slow pain (C fibres, paleospinothalamic, through the reticular formation) is dull, burning and brings nausea.
- Sensory ataxia (dorsal columns, as in vitamin B12 deficiency): steady with eyes open, falls with eyes closed (Romberg positive). Cerebellar ataxia is no better with eyes open, because vision cannot replace cerebellar function. Subacute combined degeneration adds corticospinal signs.
- A labouring woman with an epidural can be burned by a hot bottle without pain: the block has reached the spinothalamic pathway.
- Thalamus: the ventral posterolateral nucleus relays the body, the ventral posteromedial nucleus the face. A small lacunar infarct in the VPL gives contralateral loss of all sensory types in arm and leg with the face spared.
- Spinal trigeminal nucleus is arranged in rings: its caudal part serves the outer face (forehead, lateral cheek, jaw edge), the rostral part the area around the mouth and nose. A low lesion spares the perioral skin.
- Brown-Séquard (hemisection): same-side weakness and loss of vibration and position sense; opposite-side loss of pain and temperature starting about two segments below the lesion.
Matching signs to the MRI level
- The spinal cord is shorter than the vertebral column, so cord segments lie above their numbered vertebrae. In the mid-thoracic region a segment lies about two vertebrae higher: a T10 sensory level points to compression at about the T7–T8 vertebrae. Always image above the clinical level.
- A cord lesion at a given level produces upper motor neurone signs below it and lower motor neurone signs at its own segment.
- Wernicke encephalopathy (confusion, ataxia, nystagmus, sixth nerve palsy) follows glucose given without thiamine to a depleted patient (alcohol, hyperemesis, bariatric surgery): thiamine is the cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, so give it first.
Remember Repetition separates the aphasias: lost in Broca, Wernicke and conduction; kept in the transcortical types.
Exam trap Conduction aphasia leaves fluency and comprehension intact; only repetition fails.
Exam trap A sensory level on examination lies below the true level of a thoracic cord lesion on MRI.
Test yourself on this topic
5 of the 23 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Six weeks after adenoidectomy, a 7-year-old boy's speech has become very nasal, air escapes through his nose on saying 'p' and 'b', and milk sometimes comes out of his nose. He has a bifid uvula. What has failed?
Answer: Velopharyngeal closure by the soft palate
For most speech sounds and for swallowing, the soft palate rises and meets the posterior pharyngeal wall, closing off the nasopharynx; levator veli palatini is the main elevator. A submucous cleft, suggested by a bifid uvula, leaves the palate short and weak, and the bulky adenoids had been filling the gap. After their removal, air and fluid escape into the nose, giving hypernasal speech, nasal air emission on pressure consonants and nasal regurgitation.
Velopharyngeal insufficiency
- Soft palate must seal the nasopharynx
- Main elevator: levator veli palatini
- Failure: hypernasal speech
- Nasal escape and regurgitation
Remember Bifid uvula plus nasal speech after adenoidectomy: submucous cleft.
Exam trap Always look for a bifid uvula before adenoidectomy; the adenoids may be what keeps speech normal.
Why the other options are wrong
- Closure of the vocal folds Vocal fold problems change voice quality and loudness, not nasality.
- Movement of the tongue tip Tongue tip problems distort sounds like 't' and 'd' but do not make speech nasal.
- Contraction of the orbicularis oris Lip weakness affects 'p' and 'b' but does not let air into the nose.
- Elevation of the larynx by suprahyoid muscles Laryngeal elevation protects the airway; it does not seal the nasopharynx.
A 32-year-old woman with multiple sclerosis speaks slowly, breaking words into separate syllables with uneven loudness, but her vocabulary, grammar and comprehension are normal. She also has an intention tremor. Which system is responsible for this speech disorder?
Answer: Cerebellum and its connections
This is ataxic (scanning) dysarthria, a disorder of articulation rather than of language. The cerebellum coordinates the timing, force and rhythm of the muscles used in speech, so cerebellar disease breaks speech into irregular, separated syllables with variable loudness. In multiple sclerosis it results from plaques in the cerebellum or its peduncles, often with intention tremor and nystagmus. Language areas are intact, so word choice and understanding are normal.
Scanning speech
- Ataxic dysarthria
- Syllables separated, uneven
- Language normal
- Cerebellum or its peduncles
Remember Speech problem with normal language is dysarthria, not aphasia.
Exam trap Do not call slurred speech aphasia; check naming, comprehension and repetition first.
Why the other options are wrong
- Broca area of the frontal lobe Damage causes non-fluent aphasia with word-finding difficulty.
- Wernicke area of the temporal lobe Damage causes fluent speech with poor comprehension.
- Basal ganglia Basal ganglia disease gives quiet, monotonous, rapid speech.
- Arcuate fasciculus Damage causes poor repetition with normal comprehension.
After total laryngectomy for carcinoma, a 60-year-old man learns to speak again by taking air into his oesophagus and releasing it in a controlled burp. What has replaced the vocal folds as the vibrating sound source?
Answer: Pharyngo-oesophageal segment
Voice normally comes from the vocal folds, set vibrating by air from the lungs, while the pharynx, mouth and nose shape the sound into words. After laryngectomy the vocal folds are gone and the trachea opens onto the neck. In oesophageal speech, and with a tracheo-oesophageal valve, air passes up through the pharyngo-oesophageal segment, formed mainly by cricopharyngeus, which vibrates to make a new sound source. The mouth and tongue still articulate normally.
Speech production
- Normal source: vocal folds
- Articulation: tongue, lips, palate
- After laryngectomy: PE segment vibrates
- Formed mainly by cricopharyngeus
Remember Speech needs a power source, a vibrator and articulators.
Exam trap Spasm of cricopharyngeus can prevent oesophageal speech; it is sometimes divided or injected with botulinum toxin.
Why the other options are wrong
- Soft palate and uvula These shape and seal the nasopharynx; they are not the sound source.
- Tongue against the hard palate These articulate sounds but do not produce the voice.
- Lips and cheek muscles These articulate sounds but do not produce the voice.
- Oesophageal mucosa at T4 level The vibrating segment is at the pharyngo-oesophageal junction near C5–C6, not at T4.
Where are the cell bodies of the second-order neurones of the lateral spinothalamic tract, which carries pain and temperature?
Answer: Dorsal horn on the side of entry
Pain and temperature fibres (first-order neurones) have their cell bodies in the dorsal root ganglia and end in the dorsal horn of the same side, mainly in laminae I and V, within one or two segments. The second-order neurones there send axons across the midline in the anterior white commissure to form the lateral spinothalamic tract on the opposite side, which ascends to the ventral posterolateral nucleus of the thalamus (third-order neurones). This is why a central cord lesion such as syringomyelia, which damages the crossing fibres, causes bilateral loss of pain and temperature with preserved touch.
Spinothalamic pathway
- 1st: dorsal root ganglion
- 2nd: dorsal horn, same side
- Cross in anterior white commissure
- 3rd: VPL thalamus
Remember Pain crosses in the cord, near where it enters.
Exam trap Dorsal column fibres do not synapse in the cord; their second-order neurones are in the gracile and cuneate nuclei of the medulla.
Why the other options are wrong
- Dorsal root ganglion Contains the first-order neurones.
- Nucleus gracilis of the medulla Holds second-order neurones of the dorsal column pathway, not of pain.
- Ventral posterolateral thalamus Contains the third-order neurones.
- Ventral horn of the opposite side Contains motor neurones.
A man is stabbed in the back, and the left half of his spinal cord is cut at the T8 segment. He has weakness and loss of vibration and position sense in the left leg. What sensory loss is found on the right side?
Answer: Pain and temperature below about T10
Dorsal column fibres for vibration and proprioception ascend on the same side and cross in the medulla, so they are lost on the side of the lesion. Spinothalamic fibres for pain and temperature enter the cord, rise one or two segments and cross in the anterior white commissure to the opposite side. A left hemisection therefore causes loss of pain and temperature on the right from one or two segments below the lesion, with left-sided weakness and dorsal column loss.
Brown-Séquard
- Same side: weakness
- Same side: vibration, position lost
- Opposite side: pain, temperature lost
- Starts 1–2 segments below
Remember Hemisection: motor and dorsal columns same side, pain opposite.
Exam trap The level of pain loss on the opposite side is one or two segments lower than the cord lesion.
Why the other options are wrong
- Vibration and position sense in the right leg Dorsal column loss is on the side of the lesion, the left.
- Light touch only, at T8 alone Touch is carried in both pathways and is usually only reduced.
- All sensation below T8 Complete loss on one side would need more than a hemisection.
- No sensory loss on the right The crossed spinothalamic fibres are damaged, so right-sided pain loss occurs.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Nervous system and special senses, Language and speech; motor and sensory systems
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