The LMN is the motor pathway from the anterior horn cell (or cranial nerve nucleus) via a peripheral nerve to the motor end plate.
The motor unit consists of a single anterior horn cell, the single fast-conducting a motor nerve fibre that leaves the spinal cord via the anterior root, and the group of muscle fibres (100-2000) being supplied via the mixed peripheral nerve. Anterior horn cell activity is modulated by the impulses from:
• The corticospinal tracts
• The extrapyramidal system (basal ganglia and cerebellum)
• Afferent fibres from the posterior roots
Signs of lower motor neurone lesion
Voluntary muscle depends upon the motor unit for all movement and also for its metabolic integrity. Signs follow rapidly if the LMN is interrupted at any point in its course (Table 18.18). Wasting appears within 3 weeks of the development of an LMN lesion. Fasciculation occurs and is due to visible contractions of single motor units.
Causes of a lower motor neurone lesion
Examples of LM lesions at various levels are:
ANTERIOR HORN CELL-poliomyelitis, motor neurone disease
SPINAL ROOT-cervical and lumbar root lesions, neuralgic amyotrophy
PERIPHERAL (OR CRANIAL) NERVE-nerve trauma or compression, polyneuropathy
THE SPINAL REFLEX ARC
The components of the spinal reflex arc are illustrated in Fig. 18.9. The stretch reflex is the physiological basis for the tendon reflexes. For example, in the knee jerk, a tap on the patellar tendon activates stretch receptors in the quadriceps. Impulses in first-order sensory neurones pass directly to LMNs (L3 and L4), which activate the quadriceps, causing a contraction.
Loss of a tendon reflex is caused by a lesion anywhere along the spinal reflex path. The reflex lost indicates the level of the lesion (Table 18.19).
Distraction of the patient’s attention, clenching the teeth or pulling of the interlocked fingers increases the activity
of the stretch reflex. Such ‘reinforcement’ manoeuvres should be carried out before a reflex is recorded as absent.