Peripheral nerves and spinal roots
Peripheral nerves carry all modalities of sensation from either free or specialized nerve endings to the dorsal root ganglia and thus to the cord.
The sensory distribution of the spinal roots (dermatomes) is shown in Fig. 18.10
The spinal cord
Posterior columns
For clinical purposes, the sensory modalities of vibration sense, joint position, light touch and two-point discrimination travel uncrossed in the posterior columns to the gracile and cuneate nuclei in the medulla. Axons from second-order neurones cross the midline in the brain stem to form the medial lemniscus and pass to the thalamus.
Spinothalamic tracts
Fibres carrying pain and temperature sensation synapse in the dorsal horn of the cord, cross the cord and pass as the spinothalamic tracts to the thalamus and reticular formation.
The sensory cortex
The projection of fibres from the thalamus to the sensory cortex of the parietal region is shown in Fig. 18.11. Connections also exist between the thalamus and the motor cortex.
LESIONS OF THE SENSORY PATHWAYS
Paraesthesiae, numbness and pain are the principal symptoms of lesions of the sensory pathways below the level.
Peripheral nerve lesions
The symptoms are felt in the distribution of the affected peripheral nerve.
Section of a nerve is followed by complete sensory loss. Nerve entrapment (see p. 944) causes numbness, pain and tingling. Tapping the site of compression sometimes causes a sharp, electric-shock-like pain in the distribution of the nerve (Tine!’s sign).
Neuralgia
Neuralgia refers to local pain of great severity in the distribution of a damaged nerve. Examples are:
• Trigeminal neuralgia
• Postherpetic neuralgia
• Causalgia
Spinal root lesions
Root pain
The pain of root compression is referred to the myotome supplied by that root and there is also a tingling discomfort in the dermatome. The pain is made worse by manoeuvres that either stretch the nerve root (as in straight leg raising) or increase the pressure in the spinal subarachnoid space (as in coughing and straining). Cervical and lumbar disc protrusions are common causes of root lesions.
Dorsal root lesions
Section of a dorsal root causes loss of all modalities of sensation in the appropriate dermatome. However, the overlap with adjacent derma tomes may make it difficult to detect anaesthesia if only a single root is affected.
LIGHTNING PAINS. Tabes dorsalis (now a rarity) is a form of neurosyphilis that causes a low-grade inflammation of the dorsal roots and root entry zone of the cord. Its presentation includes irregular, sharp, momentary stabbing pains that involve one or two spots, typically in a calf, thigh or ankle.
Spinal cord lesions
Posterior column lesions
Posterior column lesions cause:
• Tingling of a limb
• Electric-shock-like sensations
• Clumsiness
• Numbness
• Band-like sensations
These symptoms are often felt vaguely without a clear sensory level on the side of the lesion. Position sense, vibration sense, light touch and twopoint discrimination are lost below the level of the lesion. Loss of position sense produces sensory ataxia.
LHERMITTE’s PHENOMENON. This is an electricshock- like sensation radiating down the trunk and limbs that is produced by neck flexion. It indicates a cervical cord lesion. Lhermitte’s sign is common in acute exacerbations of MS. It also occurs in cervical spondylotic myelopathy, subacute combined degeneration of the cord and radiation myelopathy.
Spinothalamic tract lesions
Pure spinothalamic lesions cause isolated contralateral loss of pain and temperature sensation below the level of the lesion. This is called ‘dissociated sensory loss’, i.e. pain and temperature are ‘dissociated’ from light touch, which is preserved. The spinal level is modified by the lamination of fibres within the spinothalamic tracts. Fibres from the lower spinal roots lie superficially and are therefore damaged first by compressive lesions from outside the cord. As an external compressive lesion (e.g. a midthoracic extradural meingioma;enlarges, the spinal sensory level ascends as deeper fibres become involved. Conversely, a central lesion of the cord (e.g. a syrinx) affects the deeper fibres first.
Symptoms of spinothalamic tract lesions are the absence of pain (resulting in painless burns and minor injuries) or the loss of temperature sensation. Perforating ulcers and neuropathic joints may follow.
Spinal cord compression
This important syndrome causes a progressive spastic paraparesis (or tetra paresis) with sensory loss below the level of the lesion. Sphincter disturbance is common. Root pain is frequent but not invariable. It is felt characteristically at the site of compression. With a lesion of the thoracic cord (e.g. an extradural meningioma), pain radiates in a band around the chest and is made worse by coughing, straining and jarring, as the meningeal sheath of the nerve is stretched.
Involvement of one spinothalamic tract (contralateral loss of pain and temperature) together with one corticospinal tract (ipsilateral ‘pyramidal’ signs) is known as the Brown-Sequard syndrome or hemisection of the cord. Paraparesis and spinal cord disease.
Pontine lesions
Pontine lesions lie above the decussation of the posterior columns. Since the medial lemniscus and spinothalamic tracts are close together, there is loss of all forms of sensation on the side opposite the lesion. The upper cranial nerve nuclei are often also involved.
Thalamic lesions
halamic lesions may produce loss of sensation to all modalities of sensation on the opposite side of the body; this is an unusual clinical picture.
Spontaneous pain may also occur. Thalamic pain, sometimes called the ‘thalamic syndrome’, is usually caused by a small thalamic infarct. The patient develops a hemiparesis that recovers partially. There remains a constant deep-seated pain that affects the paretic limbs. It is often very severe. Movement does not change the pain, which continues night and day. Extreme anguish is usual and the secondary depression that follows may lead to suicide.
Cortical lesions.
Pain is not a feature of destructive cortical lesions. Irritative phenomena (e.g. partial seizures) in the parietal cortex cause tingling sensations in the affected part. Sensory loss, neglect of one side and subtle disorders of sensation may occur with lesions of the parietal cortex.
PAIN
Pain is an unpleasant and unique physical and psychological experience. Acute pain serves a biological purpose, causes sympathetic hyperactivity and is self-limiting. Chronic pain may last for months, much longer than the time required for healing, and autonomic adaptation talces place.
The physiology of pain
Pain perception is mediated by free nerve endings, the terminations of finely myelinated AS and of non-myelinated C fibres. Chemicals released locally as a result of injury either produce pain by direct stimulation or by sensitizing the nerve endings. AS fibres give rise to the perception of sharp, immediate pain which is followed after an interval by the slower-onset, duller, more diffuse and prolonged pain mediated by the slower conducting C fibres.
Most sensory input enters the spinal cord via the dorsal spinal roots. Within the spinal cord, sensory input ascends either in the dorsal (posterior) column or in the spinothalamic tract. The cells of the grey matter in the spinal cord are arranged in laminae labelled I to X from dorsal to ventral. AS fibres terminate in laminae I and V
and excite second-order neurones which send fibres to the contralateral side via the anterior commissure and up the anterolateral column in the direct spinothalamic tract. C fibres mostly terminate in the substantia gelatinosa (laminae II and III). A series of short fibres give rise to long axons which pass through the anterior commissure to the contralateral side and up the spinoreticulothalamic tract. The spinothalamic tracts carry impulses which localize pain while thalamic pathways mediate the emotional components.
The sympathetic nervous system has an important role in modulating pain
The gate theory of pain
The gate theory proposes that the distribution of afferentv impulses is monitored by the cells of the substantia gelatinosa, which acts like a gate determining whether or not sufficient activity is allowed through to fire the secondary neurones deeper in the dorsal horn. The gate is dominated by descending influences from the brain that can override spinal cord regulatory mechanisms and alter the setting of the gate.
Endogenous opiates
Enkephalins and endorphins are neurotransmitters at inhibitory synapses. It has been suggested that the action of endogenous opiates may account for the phenomena of placebo and acupuncture analgesia
