The aim of this thesis has been to investigate the cause of the loss of tendon reflexes in a variety of clinical conditions where this sign has usually been left unexplained or given a totally unconvincing explanation. It is suggested that some of the difficulty arises from a failure to apply to this problem current neurophysiological ideas concerning the motor innervation of muscle spindles. To this end, all patients with absent tendon reflexes admitted to the wards of a neurological unit were investigated. A few additional cases were obtained from other hospitals. The series included patients with Friedreich's ataxia of 'pure' and 'mixed' forms, patients with tumours and atrophy of the cerebellum, cases of disseminated sclerosis with lesions above the level of the particular reflex involved, cases of the Holmes Adie syndrome, of Parkinsonism and of polymyositis and patients who had absent tendon -reflexes after intrathecal injection of phenol for the relief of severe spasticity. Patients with tabes dorsalis, polyneuritis, motor neurone disease and muscular dystrophy were only included to emphasise the contrast, since the areflexia in these cases has been adequately explained. The methods used included the application of a technique already applied by others to normal subjects. This involved the stimulation of the afferent fibres in the medial popliteal nerve in such a way as to cause a reflex contraction of the calf muscles. The mechanical displacement of the foot and the electromyographic response of the calf muscles following a blow on the tendo-Achilles was also recorded. It is argued that changes in both the mechanical and the electrically induced reflex are due to influences directly affecting the alpha- motorneurones while variations confined to the mechanically induced reflex suggest changes in the excitability of the stretch receptors. This technique was supplemented in some instances by motor nerve conduction studies. It is suggested that: 1) In the 'pure' forms of Friedreich's ataxia, in those rare cases of disseminated sclerosis with loss of tendon reflexes and in diseases of the cerebellum, the abnormality can be accounted for by an interruption or withdrawal of facilitatory impulses to the gamma - motorneurones, leaving the afferent side of the reflex arc intact, but that in the 'mixed' forms of Friedreich's ataxia, the lesions in the peripheral nerves are sufficient to account for the areflexia. 2) Phenytoin given in moderate doses may produce this effect on supraspinal control of the gamma-motorneurones, but if given in larger doses, it may depress synaptic transmission in the spinal cord. 3) A similar disturbance of the motor innervation of muscle spindles may also occur in Parkinsonism where there may be a depression of the monosynaptic stretch reflex with a simultaneous enhancement of the polysynaptic stretch reflexes. 4) Phenol injected intrathecally blocks the gamma - efferent fibres but in those patients who show lasting sensory disturbances there is an additional effect on the afferent fibres. 5) In some cases of polymyositis with loss of tendon reflexes in the absence of marked weakness there may be a lesion in the muscle spindles themselves or in the terminal intramuscular afferent nerve fibres, although this will require histological confirmation. 6) In tabes dorsalis and polyneuropathy the lesions in the posterior nerve roots and in the peripheral nerves are sufficient to account for the areflexia. 7) In the Holmes-Adie syndrome a disturbance of synaptic transmission in the spinal cord is postulated. 8) In motor neurone disease and muscular dystrophy, the lesion is, not surprisingly, on the motor side., Suggestions are made for further research in this field.