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VII. Groups and Details
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Or there may be awkwardness in tasks requiring ne nger movements (in handling buttons and automobile ignition keys), stiffness of the ngers, and slight weakness or wasting of the hand muscles. In other words, features related to upper and to lower motor neuron degeneration (or both) may appear insidiously in one limb. Cramping beyond what seems natural and fasciculations of the muscles of the forearm, upper arm, and shoulder girdle also appear. The earliest manifestation of the lower motor neuron component of this disease is often volitional cramping for example, leg cramps as the patient turns in bed during the early morning hours. (This is never a presenting complaint, but it is quite common as an early manifestation.) As the weeks and months pass, the other hand and arm may be similarly affected. Before long, the triad of atrophic weakness of the hands and forearms, slight spasticity of the arms and legs, and generalized hyperre exia all in the absence of sensory change leaves little doubt as to the diagnosis. Muscle strength and bulk diminish in parallel or there is a relative preservation of power early in the illness. Despite the amyotrophy, the tendon re exes are notable for their liveliness. Babinski and Hoffmann signs are variably present. Surprisingly, they may not appear even as the illness progresses. Abductors, adductors, and extensors of ngers and thumb tend to become weak before the long exors, on which the handgrip depends, and the dorsal interosseous spaces become hollowed, giving rise to the cadaveric or skeletal hand. The muscles of the upper arm and shoulder girdles are typically involved later. When an arm is the rst limb affected, all this occurs while the thigh and leg muscles seem relatively normal, and there may come a time in some cases when the patient walks about with useless, dangling arms. Later the atrophic weakness spreads to the neck, tongue, pharyngeal, and laryngeal muscles, and eventually those in the trunk and lower extremities yield to the onslaught of the disease. The affected parts may ache and feel cold, but true paresthesias, except from poor positioning and pressure on nerves, do not occur or are minor. Sphincteric control is well maintained even after both legs have become weak and spastic, but many patients acquire urinary and sometimes fecal urgency in the advanced stages of the disease. The abdominal re exes may be elicitable even when the plantar re exes are extensor. Extreme spasticity is rarely seen. Coarse fasciculations are usually evident in the weakened muscles but may not be noticed by the patient until the physician calls attention to them. Fasciculations are almost never the sole presenting feature of ALS a clinical truism with which one can reassure physicians and medical students who fear, on the basis of persistent focal muscle twitching, that they are developing the disease. The course of this illness, irrespective of its particular mode of onset and pattern of evolution, is progressive. There may be periods lasting weeks or months during which the patient observes no advance in symptoms but clinical changes can nonetheless be detected. Half the patients succumb within 3 years of onset and 90 percent within 6 years (Mulder et al). The clinical variants of motor neuron disease that occur with regularity and have distinguishing clinical features are described below. Other Patterns of Evolution In addition to the special con gurations discussed further on, there are many patterns of neuromuscular involvement other than the one just described. A leg may be affected before the hands. A foot drop with weakness and wasting of the pretibial muscles may be incorrectly attributed to peroneal nerve compression until weakness of the gastrocnemius and other muscles betrays a more widespread involvement of lumbosacral
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