Sensory and motor pathways

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Sensory and motor pathways

The central nervous system contains a large number of ascending and descending tracts that pass between the brain and spinal cord. However, in this chapter discussion will be restricted to the three most clinically important pathways that are routinely assessed in the neurological examination. The concept of upper and lower motor neurons will also be introduced, together with the anatomical basis of muscle tone and tendon reflexes.

Spinal segments

The spinal cord is divided into 31 segments (Fig. 4.1A), each with a pair of dorsal (sensory) roots and a pair of ventral (motor) roots. The dorsal and ventral roots unite on each side to form a mixed spinal nerve (spinal nerve root) (Fig. 4.1B). Each nerve root divides into a small dorsal ramus, which supplies the paravertebral muscles and provides cutaneous sensation to the back, and a large ventral ramus which innervates the limbs and trunk. The dorsal root ganglia at each spinal level contain the cell bodies of sensory neurons that innervate an area of skin called a dermatome (Fig. 4.2). They also contain the cell bodies of sensory neurons innervating muscles, tendons, ligaments and joints.

Fig. 4.1 Spinal cord segments and nerve roots.
**(A)** Schematic illustrating two spinal cord segments; **(B)** A spinal nerve root shown in transverse section. The nerve root consists of sensory and motor axons arranged in bundles (fascicles) surrounded by connective tissue (endoneurium, perineurium, epineurium) and blood vessels. Modified from Fitzgerald: Clinical Neuroanatomy and Neuroscience 5e (2006) with permission.

Fig. 4.2 Dermatomes.
**(A)** Illustration of the complete dermatome map from anterior and posterior aspects, with the spinal root values indicated; **(B)** Photograph showing a number of key dermatome levels that it is clinically-useful to be familiar with.

Internal anatomy of the spinal cord

The spinal cord has an H-shaped inner core of grey matter, with dorsal and ventral horns, surrounded by a thick layer of white matter. The ventral (anterior) horns contain longitudinal columns of motor neurons that innervate the skeletal musculature via the ventral roots; and each column supplies a functionally related group of muscles. The dorsal (posterior) horns contain sensory neurons that receive afferent projections from the dorsal root ganglia. The white matter of the spinal cord includes connections between segmental levels, together with long tracts passing to and from the brain.

Key Points

The spinal cord is divided into 31 segments, each with a pair of dorsal and ventral roots which unite on each side to form mixed spinal nerves.

The dorsal root ganglia contain the cell bodies of primary afferent neurons and provide sensation to the corresponding dermatome. The ventral roots contain efferent (motor) fibres.

The internal anatomy of the spinal cord consists of an H-shaped inner core of grey matter (arranged in dorsal and ventral horns) and an outer layer of white matter.

The spinal white matter includes connections between cord segments, together with long tracts passing to and from the brain.

Somatic sensory pathways

Two major spinal cord pathways carry sensory information to the cerebral cortex where it can be consciously perceived. The dorsal column pathway is concerned with precisely localized touch and joint position sense. The spinothalamic tract is primarily responsible for pain and temperature sensation. Each pathway is composed of a three-neuron chain with a similar arrangement (Fig. 4.3):

The first-order neurons have their cell bodies in the dorsal root ganglia, each with one process that contributes to a peripheral nerve and another that enters the spinal cord.

The second-order neurons have their cell bodies in the grey matter of the brain stem or spinal cord and give rise to axons that cross the midline, before ascending to the thalamus.

The third-order neurons are located in the ventral posterior (VP) nucleus of the thalamus and project to the primary somatosensory cortex, via the posterior limb of the internal capsule (see Ch. 3).

The axons of the somatic sensory pathways are arranged in a precise point-to-point or somatotopic fashion (Greek: soma, body; topos, place). This means that fibres innervating adjacent parts of the body surface remain side-by-side along the full length of the pathway to the brain.

Dorsal column pathway

The dorsal column pathway is mainly responsible for precisely localized touch and proprioception (awareness of one’s own body; Latin: proprius, one’s own) including joint position sense. It contains large myelinated axons (A-alpha fibres) which transmit impulses at speeds of up to 120 metres per second. Integrity of the dorsal columns is best assessed clinically using a tuning fork (Clinical Box 4.1).

Clinical Box 4.1: Testing dorsal column function

Assessment of vibration sense is the best clinical test of the dorsal column pathway. A low-frequency (128 Hz) tuning fork is applied to bony prominences and the patient (with closed eyes) is asked to report when the vibration starts and stops. Assessment of light touch and proprioception is also possible, but less reliable: a wisp of cotton wool can be applied gently to different skin areas to assess light touch; whereas joint position sense can be tested by asking the patient (again, with closed eyes) to indicate whether the examiner is flexing or extending various joints. Another indication of impaired joint position sense is difficulty standing upright with the eyes closed, which is called Romberg’s sign.

Clinical Box 4.2: Testing the spinothalamic tract

The best measure of spinothalamic tract integrity is appreciation of a mild noxious stimulus. A sterile examination pin is systematically applied to different points on the skin surface, randomly switching to the opposite (blunt) end. The patient has his or her eyes closed and is asked to say if the sensation is sharp or dull. Assessment of temperature sensitivity is impractical and is not done routinely.

Pathway to the cerebral cortex (Fig. 4.5)

The first-order neurons of the spinothalamic tract have their cell bodies in the dorsal root ganglia. The central processes enter the spinal cord where they synapse on second-order neurons in the dorsal horn.

Fig. 4.5 The spinothalamic tract.
The point at which the second order neurons cross the midline (in the anterior spinal cord) is the ventral white commissure [see text].

Axons of the second-order neurons then cross the midline in the ventral white commissure (in the anterior spinal cord) to reach the opposite side. Having crossed over, the second-order fibres ascend in the anterolateral spinal cord as the spinothalamic tract and pass through the brain stem as the spinal lemniscus. This fibre system runs in close proximity to the medial lemniscus and also terminates on third-order neurons in the thalamus.

Finally, third-order thalamocortical fibres project to the primary somatosensory cortex. It is important to note that in the spinothalamic tract (in contrast to the dorsal column pathway) axons of second-order neurons can be found crossing the midline at all levels of the cord, rather than in a single sensory decussation.

The spinoreticulothalamic pathway

Some spinothalamic axons contribute to a spinoreticular pathway which synapses in the reticular formation of the brain stem. From here, reticulothalamic fibres ascend to the intralaminar nuclei of the thalamus before projecting on to the limbic lobe and insula, which have visceral and emotional roles including pain perception (Clinical Box 4.3).

Clinical Box 4.3: Nociception versus pain

Nociception is the detection of noxious stimuli (Latin: nocēre, to harm) but its relationship to pain perception is not straightforward. For instance, soldiers injured during combat (or people involved in serious accidents) sometimes sustain devastating injuries, but feel no pain. This is termed battleground analgesia, which is regarded as a life-preserving anti-nociceptive mechanism. It is an example of stimulus-induced analgesia (another is acupuncture) and appears to rely on the release of endogenous opiates, which are similar to morphine. Conversely, some patients have intractable chronic pain syndromes with no apparent physical cause, whilst others experience pain that seems disproportionate to the degree of injury (e.g. agonising neuropathic pain following minor peripheral nerve damage). There is also a strong psychological element to pain perception. This is demonstrated by the placebo effect in which an inert substance such as a clay tablet or saline infusion can provide powerful pain relief, even in patients with serious illnesses.

Key Points

The two somatic sensory pathways have a similar organization, consisting of first-, second- and third-order neurons arranged in a linear chain.

The first-order neurons have their cell bodies in the dorsal root ganglia and central processes that enter the spinal cord via the dorsal (sensory) root.

Second-order neurons have their cell bodies in the CNS grey matter (brain stem or spinal cord) and give rise to axons that cross the midline, before ascending to the thalamus.

The third-order (thalamocortical) neurons project from the ventral posterior (VP) nucleus of the thalamus to the primary somatosensory cortex in the parietal lobe.

In the dorsal column pathway the second-order neurons are contained in the gracile and cuneate nuclei of the medulla and their axons all cross over together in the great sensory decussation.

In the spinothalamic tract the second-order neurons are located in the dorsal horns and their axons cross the midline (at all spinal cord levels) in the ventral white commissure.

Pain arising from the internal organs

The internal organs (or viscera) are insensitive to cutting and burning, but respond to stretching, twisting, inflammation and vascular compromise. Pain-related afferents from the internal organs reach the central nervous system via visceral afferent fibres which travel with autonomic nerves. Visceral pathology can generate three types of pain: visceral, viscerosomatic and referred.

Visceral and viscerosomatic pain

Visceral pain is diffuse, poorly localized and centred on the midline. It is often associated with autonomic features such as sweating, nausea, vomiting and pallor. In contrast, viscerosomatic pain is sharp and well-localized. It occurs when inflammatory exudate from a diseased organ makes contact with a somatic (body-wall) structure such as the parietal peritoneum. Abdominal pathology (e.g. appendicitis) may therefore present with diffuse visceral pain, before progressing to sharp viscerosomatic pain (Fig. 4.6).

Referred pain

This is pain that is perceived at a distance from the affected organ (e.g. in the left arm during a myocardial infarction or in the right shoulder with inflammation of the gallbladder) (Fig. 4.7). It is thought to be due to convergence of visceral and somatic afferent fibres on second-order spinothalamic tract neurons so that pain of visceral origin is perceived (‘misinterpreted’) as somatic pain at that segmental level.

In the case of cardiac pain, visceral afferents from the heart enter the thoracic cord at T1–T5 (the origin of sympathetic innervation to the heart) and pain is referred to the corresponding dermatomes of the upper limb, with radiation to the neck and jaw. In disease of the gallbladder there may be shoulder tip (C4 dermatome) pain. This is due to the embryological descent of the liver and gallbladder from the cervical region, with retention of its original segmental nerve supply.

Sensory gating and antinociception

Sensory pathways are subject to gating, meaning that impulse traffic can be facilitated or inhibited by descending influences from the brain. This can occur at any synapse in a sensory pathway, including those within the dorsal horn, medulla and thalamus.

In the spinal cord, transmission of noxious signals from first-order to second-order neurons (of the spinothalamic tract) is gated in a part of the dorsal horn known as the substantia gelatinosa. This contains excitatory and inhibitory interneurons that influence transmission of pain-related impulses to the brain. The connections are arranged in such a way that activity in large-diameter cutaneous afferents blocks transmission in nociceptive fibres, accounting for the beneficial effect of rubbing a sore knee (Fig. 4.8).

Fig. 4.8 The concept of the spinal ‘gating’ mechanism.
This is a schematic to illustrate the concept that the transmission of pain-related impulses from the spinal cord to the brain can be inhibited, either by activity in large-diameter cutaneous afferents or by descending projections from the brain stem. (NB The actual synaptic connections within the substantia gelatinosa are not certain.)

Supraspinal influences

The periaqueductal grey matter (PAG) of the midbrain is involved in the supraspinal modulation of pain. Studies in non-human primates have shown that electrical stimulation of the PAG exerts a powerful antinociceptive (analgesic) action, blocking pain signals from the spinal cord. This is mediated by connections with the reticular formation and the serotonergic raphē nuclei of the brain stem (see Ch. 1). These raphēspinal fibres synapse in the substantia gelatinosa where they inhibit synaptic transmission between first-order and second-order afferents of the spinothalamic tract (see Fig. 4.8). This partially explains why tricyclic antidepressants (e.g. amitriptyline) have analgesic properties, since they enhance serotonergic neurotransmission.

Trigeminothalamic pathways

In the head and neck, general somatic sensation is mediated by two analogous trigeminothalamic pathways. These transmit sensations from the territory of the trigeminal (V) nerve (Fig. 4.9) which is tested clinically by eliciting the corneal reflex (Fig. 4.10).

Fig. 4.9 The three branches of the trigeminal nerve provide sensation to most of the head and neck.
The trigeminal nerve also innervates the oral and nasal cavities, paranasal air sinuses, teeth, intracranial dura and cerebral arteries.

Fig. 4.10 Testing the corneal reflex.
The cornea, which is innervated by the ophthalmic division of the trigeminal nerve, is gently touched using a wisp of cotton wool. Reflexive blinking of both eyes demonstrates that the trigeminal (sensory) and facial (motor) limbs of the reflex are intact. From Munro et al.: Macleod’s Clinical Examination 10e with permission.

General tactile sensation

The cell bodies of trigeminal sensory neurons are located in the trigeminal sensory ganglion, which is analogous to a dorsal root ganglion. The second-order neurons in the trigeminothalamic pathway are located in the chief sensory nucleus of the trigeminal nerve, in the pons. This gives rise to fibres that cross the midline and ascend to the thalamus in the trigeminal lemniscus. These axons also terminate in the ventral posterior nucleus of the thalamus, medial to those from the trunk and limbs. Third-order thalamocortical neurons then project to the ‘face area’ of the primary sensory cortex (see Ch. 3).

Pain and temperature

Pain and temperature fibres originating from the head and neck (including those mediating diverse symptoms such as headache, earache and toothache) also have their cell bodies in the trigeminal ganglion. The central processes enter the brain stem via the trigeminal nerve root (in the pons) and descend to synapse in the spinal nucleus of the trigeminal nerve. This is analogous to the substantia gelatinosa and is partly contained in the upper cervical cord. Axons arising from second-order neurons in the spinal nucleus cross the midline to join the trigeminal lemniscus.

Key Points

Pain arising from the internal organs may be visceral (diffuse, central and poorly localized), viscerosomatic (sharp and well-localized) or referred.

Referred pain is perceived at a distance from the affected organ. Impulses from visceral afferent fibres are ‘misinterpreted’ as somatic pain at the corresponding segmental level.

Like other sensory projections, the central pain pathways are subject to gating. This means that supraspinal influences (from the brain) can facilitate or inhibit ascending signals.

Pain from the head and neck region is transmitted from the territory of the trigeminal nerve via the trigeminothalamic system.

The second-order neurons have their cell bodies in the spinal nucleus of the trigeminal nerve, which is analogous to the substantia gelatinosa in the dorsal horn of the spinal cord.

Somatic motor pathways

The control of voluntary movement is complex and incompletely understood, with contributions from several brain regions (see Ch. 3). The prefrontal cortex, which lies anterior to the motor and premotor areas of the frontal lobe, is involved in planning and organization of goal-directed behaviour. The premotor cortex is concerned with the preparation and execution of complex movement sequences, whereas the primary motor cortex has a more direct influence over individual muscle groups.

The primary motor pathway has two components. The corticospinal tract originates in the motor and premotor areas of the frontal lobe and projects to the spinal cord to control the limb and trunk muscles. The corticobulbar pathway also originates in the motor and premotor cortex but only descends as far as the brain stem, where it influences the cranial nerve motor nuclei. The primary motor pathway is also referred to as the pyramidal motor system (or pyramidal tract) because the corticospinal tract passes through the pyramids of the medulla. Interruption of the pyramidal tract causes weakness or paralysis.

Corticospinal tract

The corticospinal tract is the principal somatic motor pathway and the longest continuous white matter tract in the CNS. It is particularly important for finely-fractionated voluntary movements of the distal limb musculature (e.g. control of the hands). The corticospinal tract is composed of more than a million myelinated axons on each side, two thirds of which arise from the primary motor and premotor areas of the frontal lobe (Fig. 4.11).

The remaining third of fibres originate from the primary somatosensory cortex in the parietal lobe and synapse in the dorsal (sensory) horn of the spinal cord. This part of the corticospinal pathway is not directly involved in movement initiation, but is thought to be important for ‘filtering out’ the barrage of proprioceptive and other sensory information generated by complex movements. By predicting and filtering out these afferent impulses, the brain is able to increase the ‘signal-to-noise’ ratio and focus on more important or unexpected sensory feedback.

Origin, course and destination (Fig. 4.12)

Corticospinal tract axons leave the cerebral cortex to enter the subcortical white matter, passing through the posterior limb of the internal capsule to reach the crus cerebri in the anterior midbrain.

Having traversed the crus cerebri and basilar pons, the corticospinal fibres enter the medulla where they occupy the anterior midline as the pyramids. At the lower border of the medulla, 75–90% of the pyramidal fibres decussate to enter the contralateral half of the spinal cord.

The pathway continues as the lateral corticospinal tract, which predominantly supplies the distal limb musculature (particularly the flexor groups). The 10–25% of uncrossed fibres are a direct continuation of the medullary pyramids. They therefore descend in the anterior part of the spinal cord on either side of the midline (as the anterior corticospinal tract). Many of these fibres eventually decussate and chiefly innervate the proximal and axial musculature (particularly the extensor groups).

Only a small proportion of corticospinal tract axons make direct synaptic contact with spinal motor neurons (mainly those supplying the intrinsic muscles of the hands). The majority terminate on interneuronal pools which influence spinal motor neurons indirectly.

Corticobulbar tract

The corticobulbar tract arises in the cerebral cortex and projects to the brain stem (the word ‘bulb’ is an archaic term for the lower brain stem). The projections arise mainly from the ‘face’ and ‘tongue’ areas of the primary motor and premotor cortices. The corticobulbar (or corticonuclear) projections accompany the corticospinal tract as far as the brain stem. They pass in turn through the subcortical white matter and internal capsule to reach the crus cerebri of the midbrain where they lie just medial to the corticospinal fibres.

Termination of corticobulbar fibres

Fibres from the corticobulbar projection part company with the corticospinal tract as they descend in the brain stem and gradually ‘peel off’ to reach their target nuclei. The corticobulbar tract projects directly to four motor cranial nerve nuclei in the pons and medulla, controlling muscles that: (i) are attached to the lower jaw, including those involved in chewing; (ii) are involved in facial expression; (iii) mediate speech, swallowing and the efferent limb of the ‘gag’ reflex (see Clinical Box 4.4); and (iv) control the tongue.

Clinical Box 4.4: The gag reflex

To test this reflex (e.g. during a routine neurological examination) a wooden tongue depressor is used to touch the posterior pharyngeal wall on each side. The normal response is a ‘gag’, with elevation of the soft palate and uvula. The afferent (sensory) limb is subserved by the glossopharyngeal (IX) nerve which supplies sensation to the pharynx and posterior tongue. The efferent (motor) limb is mediated by the vagus (X) nerve which supplies the muscles of the larynx and pharynx.

Voluntary eye movements are initiated by the frontal eye fields (see Ch. 3). These project to vertical and lateral gaze centres in the midbrain and pons, via the anterior limb of the internal capsule. The brain stem gaze centres then influence the cranial nerve nuclei innervating the extraocular muscles.

Decussation of bulbar fibres

Most of the cranial nerve motor nuclei receive projections from both cerebral hemispheres, so that damage on one side of the brain tends not to cause contralateral bulbar weakness. Exceptions are the cortical projections controlling the tongue and the lower part of the face, which arise mainly from the opposite motor cortex. This explains why isolated lower facial paralysis sometimes occurs after a stroke (the upper part of the face is spared since it is also controlled by the opposite cerebral hemisphere).

Key Points

The primary motor (pyramidal) pathway consists of the corticospinal and corticobulbar tracts which mainly originate from the motor and premotor areas of the frontal lobe.

The corticospinal tract descends through the internal capsule, crus cerebri of the midbrain, basilar pons and medullary pyramids.

At the lower border of the medulla, 75–90% of corticospinal tract fibres cross the midline to enter the lateral corticospinal tract of the spinal cord.

The corticobulbar pathway accompanies the corticospinal fibres as far as the brain stem before peeling off to innervate the cranial nerve motor nuclei (bilaterally in most cases).

Lower motor neurons

The term lower motor neuron is used clinically to describe the motor neurons of the spinal cord and brain stem that innervate the skeletal musculature. In contrast, the term upper motor neuron refers to corticospinal and corticobulbar tract neurons which have their cell bodies in the motor cortex of the frontal lobe.

Lower motor neurons of the spinal cord have their cell bodies in the anterior horns and are therefore also called anterior horn cells. The alternative term alpha motoneuron reflects their large-diameter A-alpha axons, which conduct nerve impulses at high speeds. The lower motor neuron is described as the ‘final common pathway’ since it is the route by which all motor activity (both voluntary and reflexive) is initiated.

Motor units and graded contraction

A motor unit consists of a single anterior horn cell and the squad of muscle fibres that it supplies. Motor units operate in an ‘all-or-none’ fashion so that muscle contraction can only be graded by the recruitment of whole numbers of motor units. Muscles capable of precise, finely-fractionated movements therefore have small motor units. Those that supply the intrinsic muscles of the hand typically have fewer than 10 muscle fibres, whereas the motor units of the limb-girdle and axial muscles may be composed of 1000 fibres or more.

In order to increase the force of contraction in a muscle, motor units are gradually recruited according to the size principle. This refers to the fact that small motor units (commanding fewer muscle fibres) are recruited before larger ones. This happens automatically since small neurons are more easily depolarized and means that movements requiring minimal force can be more finely graded.

The neuromuscular junction

The point of contact between lower motor neurons and skeletal muscle is the neuromuscular junction (NMJ) which is similar in structure to a synapse (Fig. 4.13). The transmitter is acetylcholine (ACh) which acts on nicotinic ACh receptors. The NMJ is ‘fail-safe’, meaning that 100% of nerve impulses generated in a lower motor neuron will trigger a muscle twitch. Neuromuscular transmission is impaired in the autoimmune disorder myasthenia gravis (Clinical Box 4.5).

Clinical Box 4.5: Myasthenia gravis

This is a rare autoimmune disease caused by autoantibodies to the nicotinic acetylcholine receptor at the neuromuscular junction. It is characterized by fatigable weakness, meaning that symptoms worsen with use and improve with rest. It is more common in females and approximately three-quarters of patients have an abnormality of the thymus gland. This is most often thymic hyperplasia (increase in the size and activity of the gland) but in 10% of cases there is a benign tumour called a thymoma. Although myasthenia gravis cannot be cured, it can be managed using agents that (i) block degradation of acetylcholine or (ii) suppress the autoimmune response.

Fig. 4.13 The neuromuscular junction (motor end plate).

Key Points

Lower motor neurons (with cell bodies in the anterior horn of the spinal cord or cranial nerve motor nuclei) represent the ‘final common pathway’ by which all movements are mediated.

Axons of lower motor neurons travel in peripheral nerves and make contact with skeletal muscle at the neuromuscular junction, which uses the neurotransmitter acetylcholine.

A lower motor neuron and the squad of muscle fibres that it innervates constitutes a motor unit. Dextrous muscles (e.g. those of the hands) have smaller motor units.

Muscle contractions are graded by the recruitment of motor units according to the size principle: small motor neurons (commanding fewer muscle fibres) are recruited before larger ones.

Reflexes and muscle tone

A reflex is a stereotyped motor response to a particular stimulus that may vary in latency, duration or amplitude. The simplest type is monosynaptic and is composed of a single afferent neuron, a single efferent neuron and an intervening synapse. Some reflexes are polysynaptic and may extend over several spinal segments to produce more complex responses.

Muscle tone

Muscles exhibit a degree of rest tone which helps maintain normal posture and joint stability. This can be appreciated on clinical examination as mild resistance to passive joint flexion and extension. Rest tone is not an intrinsic property of muscle but is mediated by the stretch reflex. This is a simple monosynaptic reflex which enables muscles to contract automatically in response to being stretched, thereby resisting passive changes in length.

The stretch reflex

The afferent limb of the stretch reflex originates from proprioceptive organs called muscle spindles (Fig. 4.14). These are roughly the same size and shape as a grain of rice and are scattered throughout the skeletal musculature. They contain striated muscle within a spindle-shaped (fusiform) connective tissue capsule. Muscle fibres inside the spindle are referred to as intrafusal, whereas those making up the bulk of the muscle are extrafusal. Muscle spindles are in parallel with extrafusal fibres, so that any tension applied to the long axis of the muscle will stretch both types of fibre.

Muscle spindles are richly innervated by mechanosensitive nerve endings which terminate in the non-contractile central portion of the fibres. These nerve endings are exquisitely sensitive to changes in muscle fibre length, particularly the rate of change of length. A short, sharp stretch is therefore a better stimulus than sustained tension.

Afferent fibres enter the dorsal roots of the spinal nerves, then synapse directly on anterior horn cells innervating the homonymous (same) muscle group (Fig. 4.15). In addition, collateral fibres make synaptic connections with motor neurons supplying antagonistic muscle groups via inhibitory interneurons. The stretch reflex is fundamentally important in clinical neurology because it is responsible for muscle tone and tendon reflexes (Clinical Box 4.6).

Clinical Box 4.6: Tendon reflexes

Tendon reflexes are elicited by striking a tendon with a patellar hammer. This stretches the muscle and triggers a volley of afferent impulses from its muscle spindles. Reflexive contraction of the muscle is combined with reciprocal inhibition of its antagonists, seen as a brief ‘jerk’ of the limb (e.g. knee extension after striking the patellar tendon). Abnormal reflexes help to localize lesions to a particular spinal root level (e.g. biceps reflex: C5/C6; patellar reflex: L3/L4). Increase in the speed or amplitude of a reflex is termed hyperreflexia and the response is described as brisk. A reduced (or absent) response is referred to as hyporeflexia (or areflexia). It is normal for reflexes to vary from person to person, but asymmetry is usually a sign of pathology.

The gamma loop

Intrafusal muscle fibres have a separate motor innervation that arises from gamma motoneurons (also located in the anterior horn). These neurons co-activate with alpha motoneurons to ensure that the intrafusal fibres remain under tension (do not become slack) when muscles contract, so that stretch-sensitivity is maintained during movements.

Long-latency stretch reflex

Electrical recordings from muscle show that the stretch reflex has two components. There is an early, short-latency component that occurs within 25–40 milliseconds, consistent with a monosynaptic reflex. A long-latency component can also be recorded at around 50–75 milliseconds, which probably involves the cerebral cortex. Over-activity in the ‘long-loop component’ of the stretch reflex may be responsible for the characteristic rigidity (increased muscle tone) in Parkinson’s disease (Ch. 13).

Hypertonia and spasticity

Sensitivity of the stretch reflex is regulated by the brain to ensure normal muscle tone. Descending reticulospinal projections (from the reticular formation of the brain stem) inhibit spinal motor neurons and ‘damp down’ the stretch reflex to optimize muscle tone. This influence is usually lost following an upper motor neuron lesion (by an uncertain mechanism) which results in hyperactivity of the stretch reflex (Clinical Box 4.7).

Clinical Box 4.7: Upper and lower motor neuron lesions

In an upper motor neuron (UMN) lesion such as a stroke, weakness is associated with features that reflect hyperexcitability of the stretch reflex. These include hypertonia, hyperreflexia and spasticity, with clasp-knife rigidity. The typical clinical features take several days to evolve and are preceded by an initial period of flaccid paralysis (perhaps due to loss of descending excitatory projections from the cortex, followed by a subsequent increase in lower motor neuron sensitivity). In a lower motor neuron (LMN) lesion such as a peripheral nerve injury, there is partial or complete denervation of the affected muscles. This leads to weakness, wasting and areflexia (or flaccid paralysis in severe cases). Visible muscle twitches called fasciculations may also be seen, caused by random spontaneous discharge of individual motor units.

Spasticity

A marked increase in muscle tone is called spasticity (Fig. 4.16), characterized by firm resistance to passive manipulation of the limbs. It is velocity-dependent, so that rapid flexion or extension of the affected joints is met by an abrupt ‘spastic catch’ (similar to the resistance felt when pulling sharply on a car seatbelt). Spasticity can be overcome by force so that the joint suddenly ‘gives way’ (the clasp-knife phenomenon). This is a safety mechanism that prevents tendon rupture due to excessive load. Spasticity is usually accompanied by an abnormal plantar response (Clinical Box 4.8). A combination of upper motor neuron features, together with lower motor neuron signs, is seen classically in motor neuron disease (Clinical Box 4.9).

Clinical Box 4.8: The plantar response