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hyperre exic state, such as the Hoffmann sign and the crossed adductor re ex of the thigh muscles Also, re exes may be inverted, as in the case of a lesion of the fth or sixth cervical segment; here the biceps and brachioradialis re exes are abolished and only the triceps and nger exors, whose re ex arcs are intact, respond to a tap over the distal radius In addition to hyperactive phasic myotatic re exes ( tendon jerks ), certain lesions, particularly of the cervical segments of the spinal cord, may result in great enhancement of tonic myotatic re exes These are stretch re exes in which a stimulus produces a prolonged asynchronous discharge of motor neurons, causing sustained muscle contraction As the patient stands or attempts voluntary movement, the entire limb may become involved in intense muscular spasm, sometimes lasting for several minutes During this period the limb is quite useless Presumably there is both an interruption of lateral reticulospinal inhibitory in uences on the anterior horn cells and a release of the medial reticulospinal facilitatory effects needed in antigravity support (Henneman) With bilateral cerebral lesions, exaggerated stretch re exes can be elicited in cranial as well as limb and trunk muscles because of interruption of the corticobulbar pathways These are seen as easily triggered masseter contractions in response to a brisk downward tap on the chin (jaw jerk) and brisk contractions of the orbicularis oris muscles in response to tapping the philtrum or corners of the mouth In advanced cases, weakness or paralysis of voluntary movements of the face, tongue, larynx, and pharynx are added (bulbar spasticity or pseudobulbar palsy; see pages 426 and 445) There have been many investigations of the biochemical changes that underlie spasticity and the mechanisms of action of antispasticity drugs These have been reviewed by Davidoff Since glutamic acid is the neurotransmitter of the corticospinal tracts, one would expect its action on inhibitory interneurons to be lost As mentioned earlier, gamma-aminobutyric acid (GABA) and glycine are the major inhibitory transmitters in the spinal cord; GABA functions as a presynaptic inhibitor, suppressing sensory signals from muscle and cutaneous receptors Baclofen, a derivative of GABA, as well as diazepam and progabide, are thought to act by reducing the release of excitatory transmitter from the presynaptic terminals of primary afferent terminals Actually, none of these agents is entirely satisfactory in the treatment of spasticity when administered orally; the administration of baclofen intrathecally may have a more bene cial effect Glycine is the transmitter released by inhibitory interneurons and is measurably reduced in quantity, uptake, and turnover in the spastic animal There is some evidence that the oral administration of glycine reduces experimentally induced spasticity, but its value in patients is uncertain Interruption of descending noradrenergic, dopaminergic, and serotonergic bers is undoubtedly involved in the genesis of spasticity, although the exact mode of action of these neurotransmitters on the various components of spinal re ex arcs remains to be de ned Table 3-1 summarizes the main attributes of upper motor neuron lesions and contrasts them with those of the lower motor neuron.

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Myopathic Fatigue Not unexpectedly, fatigue and intolerance of exercise (ie, fatigue with mild exertion) are prominent manifestations of myopathic disease, in which muscles are weak to begin with Even in a disease such as myasthenia gravis, the muscles exhibiting fatigue are usually weak even in the resting state The classes of myopathic disease in which weakness, inability to sustain effort, and excessive fatigue are notable features include the following: the muscular dystrophies, congenital myopathies, disorders of neuromuscular transmission (myasthenia gravis, Lambert-Eaton syndrome), toxic myopathies (eg, due to cholesterol-lowering drugs), some of the glycogen storage myopathies, and mitochondrial myopathies One type of glycogen storage disease McArdle phosphorylase de ciency is exceptional in that fatigue and weakness are accompanied by pain and sometimes by cramps and contracture The rst contractions after rest are of near normal strength, but after 20 to 30 contractions, there occurs a deep ache and an increasing rmness and shortening of the contracting muscles The characteristics of these diseases are presented in the chapters on muscle disease Another such process acid maltase de ciency is at times associated with disproportionate weakness and fatigue of respiratory muscles, which leads to dyspnea and retention of carbon dioxide Fatigue in Neurologic Diseases Fatigue of varying degree is a regular feature of all diseases that are marked by denervation of muscle and loss of muscle ber Fatigue in these cases is due to the excessive work imposed on the intact muscle bers (overwork fatigue) This is most characteristic of amyotrophic lateral sclerosis and the postpolio syndrome, but it also occurs in patients who are recovering from Guillain-Barre syndrome and in those with chronic polyneuropathy Not surprisingly, many neurologic diseases that are characterized by incessant muscular activity (Parkinson disease, double athetosis, Huntington disease, hemiballismus) induce fatigue Also, muscles partially paralyzed by a stroke feel tired and may cause overall fatigue state (the distinguished neuroanatomist A Brodal has given an interesting account of his own stroke and its effects on muscle power) Fatigue is often a major complaint of patients with multiple sclerosis; its cause is unknown, although the effect of interleukins circulating in the cerebrospinal uid has been pos-.

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