Book pp. 1037–1039 · asked 3 times in NTRUHS papers

In one breath

The pattern of sensory loss tells you where a lesion lies, from a single nerve up through the roots, ganglia, spinal cord, brainstem and thalamus to the cortex. In the cord, fine touch, position and vibration climb the dorsal column of the same side, while pain and temperature cross over and climb the opposite anterolateral system, so a hemisection (Brown-Séquard syndrome) splits the loss between the two sides. A medullary lesion gives crossed loss (face on one side, body on the other), a thalamic lesion gives thalamic syndrome, and a cortical lesion takes away localization, two-point discrimination and stereognosis. Sensory function is tested by clinical examination, sensory nerve conduction and somatosensory evoked potentials.

Builds on: Ascending tracts: dorsal column and anterolateral system · Abnormalities of dorsal column sensations · Thalamus: nuclei, functions and thalamic syndrome · Somatosensory cortex · Leads to: Corticospinal (pyramidal) tract · Upper vs lower motor neuron lesions

Localizing a sensory lesion

Knowing how the sensory system normally works is what lets a clinician diagnose and manage its disorders.

  • Two things must be found: the nature of the deficit, and its level along the sensory pathway (the sensory neuraxis).
  • Both are read from the distribution and the type of sensory loss.
  • Disease can strike the nerve, nerve root, spinal cord, brainstem, thalamus or cortex.
  • How bad the deficit is depends on the site of the lesion, the kind of disease and its severity.

Nerve, root and ganglion lesions

Single peripheral nerve

What a nerve lesion does depends on whether the nerve is mainly cutaneous, muscular or mixed.

  • A cutaneous nerve lesion numbs the skin that nerve supplies.
  • The numb area is always smaller than the nerve’s anatomical territory, because neighbouring nerves overlap into it.
  • Deep pressure and passive movement are usually still felt: they are carried by fibres from subcutaneous tissue and joints.
  • Compression picks off fibres by size:
FibresCarryWhen compressed
LargeTouch, pressureAffected
SmallPain, temperatureSpared

Polyneuropathy

Polyneuropathy means many nerves are damaged at once. The common kinds are diabetic, inflammatory and vasculitic neuropathies, and the loss is usually on both sides.

  • The longest, largest fibres suffer most, so the loss is worst in the legs and feet, and in the hands.
  • All modalities are lost. A distal, symmetrical loss gives glove-and-stocking anesthesia: both hands and both feet.
  • If the damage is more demyelinating than axonal, paresthesia is an early feature.
  • The large kinesthetic fibres, for position and vibration, are hit hardest, so sensory ataxia may develop.
  • In chronic cases the long-standing loss of pain lets trophic ulcers form.

Applied: the diabetic foot

Diabetic neuropathy is one of the commonest polyneuropathies. Once the feet have lost pain sense, small injuries and pressure go unnoticed, and the trophic ulcers that follow are a major reason for amputation. Worth knowing, though not in your pages: this is why diabetics are taught to inspect their feet every day.

Nerve root lesion (radiculopathy)

  • A root lesion causes segmental anesthesia: loss over the dermatome of the cord segment that root comes from.
  • The usual cause is compression of a single sensory root by a herniated intervertebral disc.
  • Neighbouring roots overlap heavily, so one root lesion never leaves any patch of skin completely numb.

Sensory ganglia

  • The dorsal root ganglia are damaged in many inflammatory, toxic and neoplastic diseases.
  • The loss is like that of a root lesion, but more marked in the proximal parts of the body.

Spinal cord lesions

The syndrome depends on which part of the cord the disease destroys.

SyndromePart damagedMain loss
TabeticOne dorsal columnPosition, vibration
Posterior columnBoth dorsal columnsPosition, vibration
Brown-SéquardOne half of the cordSplit between the sides
CompleteWhole cross-sectionAll, below the level
SyringomyelicAround the central canalPain, temperature
Anterior spinal arteryVentral halfPain, temperature, power

The key to all of them: dorsal column fibres (fine touch, proprioception, two-point discrimination) ascend on the same side, while pain and temperature fibres cross and ascend in the anterolateral system of the opposite side.

Tabetic syndrome

  • In tabes dorsalis, the large proprioceptive and other posterior column fibres are destroyed; your book draws this on one side.
  • Position and vibration sense are lost. Numbness and paresthesia may occur, and Romberg sign may be positive (see Abnormalities of dorsal column sensations).
  • The typical cause is neurosyphilis, but the same picture occurs in diabetes.

A slip in your book: tabes is not one-sided

Your book pictures tabetic syndrome as a lesion of one dorsal column, which is how it keeps it apart from the two-sided posterior column syndrome. Give that answer when asked. Worth knowing, though not in your pages: tabes dorsalis itself usually damages the dorsal roots and dorsal columns on both sides. A positive Romberg sign fits this, since your book’s ascending pathways chapter ties it to lost position sense in both legs.

Posterior column syndrome

  • Both dorsal columns are destroyed.
  • Vibration and position sense are lost, while pain and temperature are spared.
  • Stereoanesthesia, impaired graphesthesia and impaired tactile sensibility also occur.
  • It looks like a cortical lesion, and your book says the loss of vibration is what tells them apart.

Stereoanesthesia is not astereognosis

Both mean failing to recognize an object by touch. In stereoanesthesia (cord or brainstem lesion) the touch and position signals never reach the brain. In astereognosis (cortical lesion) the primary touch sense is intact, but the cortex cannot put it together. Your book’s ascending pathways chapter draws this line (see Abnormalities of dorsal column sensations).

Brown-Séquard syndrome

This is the result of hemisection of the spinal cord, usually from injury or a tumour involving only one half of the cord. It is named after Charles-Édouard Brown-Séquard (1817–1894), who described how the spinal tracts conduct. He also showed that the adrenal glands are essential to life.

WhereLost below the lesion
Same sideFine touch, proprioception, vibration
Same sideTactile discrimination
Same sidePower: paresis with spasticity
Opposite sidePain and temperature
  • Why the sensory loss splits: fine touch, proprioception and two-point discrimination travel up the dorsal column of the same side, so they are lost on the side of the cut. Pain and temperature have already crossed to the opposite anterolateral system, so they are lost on the other side.
  • Why the weakness is on the same side: the hemisection cuts that side’s Corticospinal (pyramidal) tract, giving paresis and spasticity of the same side of the body (see Upper vs lower motor neuron lesions).
  • Worth knowing, though not in your pages: at the level of the lesion there is also a narrow band of loss of all sensation on the same side, with lower motor neuron weakness of the muscles of that segment, and often a strip of hyperesthesia just above it. The opposite-side loss of pain and temperature starts one or two segments below the lesion, because those fibres climb a little before they cross. The same-side tendon reflexes are brisk and the plantar response is extensor (Babinski sign).

Complete transection

  • Every form of sensation is abolished below the level of the lesion.
  • A narrow band of hyperesthesia usually lies at the upper margin of the numb zone.

Syringomyelic syndrome

  • In syringomyelia the lesion lies around the central canal.
  • It cuts the lateral spinothalamic fibres (pain and temperature) as they cross, but leaves the dorsal column fibres alone.
  • So pain and temperature are lost while touch and position sense survive: dissociated sensory loss. Your book’s ascending pathways chapter explains the anatomy (see Abnormalities of dorsal column sensations).
  • Worth knowing, though not in your pages: the cavity is commonest in the cervical cord, so the loss often lies like a cape over the shoulders and arms, on both sides, over just the segments the cavity spans.

Anterior spinal artery syndrome

  • The anterior spinal artery supplies the ventral part of the cord. If it is blocked or bleeds, the anterior half of the cord infarcts: anterior myelopathy.
  • Below the lesion, pain and temperature are lost, but proprioception is spared.
  • Spastic paralysis follows, because the corticospinal tracts are involved.
  • Worth knowing, though not in your pages: most books say the artery supplies the anterior two-thirds of the cord. The dorsal columns are fed by the posterior spinal arteries, which is why proprioception survives.

Draw it: the six cord lesions

Draw six small cord cross-sections, each with its H-shaped grey matter and central canal. Shade: (A) one dorsal column, for tabetic syndrome; (B) both dorsal columns, for posterior column syndrome; (C) one whole half, for Brown-Séquard; (D) the whole section, for complete transection; (E) a ring around the central canal, catching the crossing fibres, for syringomyelia; (F) the front half of both sides, for anterior spinal artery syndrome. For a Brown-Séquard answer, draw (C) large and label, on the cut side, the dorsal column, the lateral spinothalamic tract and the lateral corticospinal tract. Beside it, draw a body outline shading same-side touch and position loss and opposite-side pain and temperature loss.

Brainstem lesions

The pattern depends on where along the brainstem the lesion is.

  • Medulla: a one-sided lesion catches the descending (spinal) tract of the trigeminal nerve and the already crossed lateral spinothalamic tract together. The result is crossed sensory loss: pain and temperature are lost over one side of the face and the opposite side of the body.
  • Upper medulla, pons and lower midbrain: by this height the crossed spinothalamic bundle and the trigeminothalamic fibres travel together. A lesion here takes pain and temperature from the face and the body of the other side, while every other sensation survives, since the medial lemniscus lies apart and escapes.
  • Upper brainstem: the spinothalamic tract and medial lemniscus have merged, so a lesion removes all superficial and deep sensation from the opposite side.
  • Worth knowing, though not in your pages: in the crossed pattern the face loss is on the side of the lesion, since the trigeminal tract has not crossed (see Trigeminal pathway and trigeminal neuralgia). The classic example is the lateral medullary syndrome from thrombosis of the posterior inferior cerebellar artery, which your book’s ascending pathways chapter lists among the causes of dissociated anesthesia.

Thalamic lesions

  • A severe, widespread thalamic lesion blunts every sensory modality over the contralateral half of the body.
  • The pain threshold may rise, yet a mildly painful stimulus can bring an exaggerated response; your book calls this hyperalgesia.
  • Touch itself may feel unpleasant, which your book calls paresthesia.
  • This is thalamic syndrome, and it follows lesions of the lateral and ventral nuclei (see Thalamus: nuclei, functions and thalamic syndrome).
  • Worth knowing, though not in your pages: a raised threshold with an exaggerated, unpleasant response once it is crossed is usually called hyperpathia. Your book’s ascending pathways chapter uses hyperpathia and hyperesthesia as the same thing, and names thalamic lesions as a cause.

Cortical lesions

The cortex handles the finer side of sensation, above all its spatial and discriminative aspects.

  • That is why tactile localization, two-point discrimination and stereognosis are called the cortical sensations.
  • A cortical lesion causes:
    • topagnosia: touch and pain cannot be localized;
    • astereognosis;
    • wider two-point discrimination;
    • impaired proprioception and vibration sense.
  • Sensory inattention, extinction or neglect is the hallmark of a parietal lobe lesion (see Somatosensory cortex).

Vibration: your book says two things

The posterior column section says loss of vibration is what separates a posterior column lesion from a cortical one. This section, and the ascending pathways chapter, say vibration is impaired in cortical lesions too. Worth knowing, though not in your pages: the usual clinical teaching is that vibration is lost in dorsal column lesions but largely spared by cortical ones, so the safer exam line is that marked loss of vibration points to the cord.

Sensory function tests

Three kinds of test assess the sensory system: clinical examination, sensory nerve conduction studies and somatosensory evoked potentials.

Clinical examination

  • A thorough examination should establish the nature and the level of the sensory loss.
  • Test every modality over every dermatome of the body, one by one. The method is in your practical physiology book.
  • Worth knowing, though not in your pages: the usual bedside tools are a wisp of cotton (fine touch), a pin (pain), warm and cold tubes (temperature), a 128 Hz tuning fork (vibration), passive movement of a finger or toe (position) and a blunt divider (two-point discrimination).

Sensory nerve conduction

  • Electrophysiological studies help to confirm the diagnosis.
  • Analysing the sensory nerve action potential and measuring conduction velocity diagnoses sensory neuropathy.
  • Recording the H and F responses helps detect radiculopathy.

Somatosensory evoked potentials

  • Somatosensory evoked potentials (SEP) show conduction defects in large-diameter fibres anywhere along the peripheral nerve, brainstem, thalamus and cortex.
  • They are especially useful for deciding whether a defect is in the peripheral or the central pathway.
  • Worth knowing, though not in your pages: a peripheral nerve (such as the median at the wrist) is stimulated repeatedly, and averaged responses are recorded over the spine and scalp.

Exam-answer skeleton: "Brown-Séquard syndrome" (short note)

  1. Definition: the effects of hemisection of the spinal cord, named after Brown-Séquard.
  2. Causes: spinal cord injury, or a tumour involving one half of the cord.
  3. Diagram: a cord cross-section with one half shaded, labelling the dorsal column, lateral spinothalamic and lateral corticospinal tracts.
  4. Same-side loss below the lesion: fine touch, proprioception, vibration and tactile discrimination.
  5. Opposite-side loss below the lesion: pain and temperature.
  6. Motor: paresis and spasticity on the same side, from corticospinal damage.
  7. The basis: dorsal column fibres ascend uncrossed, while pain and temperature fibres cross to the opposite anterolateral system.
  8. If time allows, the signs at the level: a band of total sensory loss with lower motor neuron weakness, and hyperesthesia just above.

Asked in exams