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Often there is a sudden burst of words, without meaning or relevance to what was just said Such an outburst may terminate the attack, for which there is complete or nearly complete amnesia In many respects the attacks resemble episodes of nocturnal sleepwalking Such attacks of automatic behavior and amnesia are common, occurring in more.

This is characteristic of intoxication with alcohol, sedative drugs, and anticonvulsants. The drunken patient totters, reels, tips forward and then backward, appearing each moment to be on the verge of losing his balance and falling. Control over the trunk and legs is greatly impaired. The steps are irregular and uncertain. Such patients appear stupe ed and indifferent to the quality of their performance, but under certain circumstances they can momentarily correct the defect. As indicated above, the adjectives drunken and reeling are used frequently to describe the gait of cerebellar disease, but the similarities between them are only super cial. The severely intoxicated patient reels or sways in many different directions and seemingly makes little or no effort to correct the staggering by watching his legs or the ground, as in cerebellar or sensory ataxia. Also, the variability of the drunken gait is noteworthy. Despite wide excursions of the body and deviation from the line of march, the drunken patient may, for short distances, be able to walk on a narrow base and maintain his balance. In contrast, the patient with cerebellar gait has great dif culty in correcting his balance if he sways or lurches too far to one side. Milder degrees of the drunken gait more closely resemble the gait disorder that follows loss of labyrinthine function (see earlier discussion).

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(a) Code: {0, 10, 11} (b) Code: {0, 1, 00} (c) Code: {10, 01, 00}

ticospinal tract disorder that begins with a pure spastic paraparesis; later, and to a lesser degree, the arms and oropharyngeal muscles become involved These cases have distinctive neuropathologic features and are designated as primary lateral sclerosis, a term originally suggested by Erb in 1875 A historical review of the subject appears in the article by Pringle and colleagues The features that most distinguish these cases from hereditary spastic paraparesis (HSP) is the onset during adulthood and the involvement of the arms and oropharyngeal muscles; the latter are almost universally spared in HSP The typical case begins insidiously in the fth or sixth decade with a stiffness in one leg, then the other; there is a slowing of gait, with spasticity predominating over weakness as the years go on.

Walking is still possible with the help of a cane for many years after the onset, but eventually this condition acquires the characteristic features of a severe spastic paraparesis Over the years, nger movements become slower, the arms become spastic, and, if the illness persists for decades, speech takes on a pseudobulbar tone In some patients the illness evolves over a few years There are no sensory symptoms or signs The legs are often found to be surprisingly strong, the dif culty in locomotion being attributable mainly to rigid spasticity About half the patients acquire spasticity of the bladder Pringle and associates suggest that an important diagnostic criterion of the disease is progression for 3 years without evidence of lower motor neuron dysfunction A rare type begins in the oropharyngeal muscles, as mentioned above, but almost always, atrophy and fasciculations in this same region are evident within months.

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Laboratory studies are seldom helpful In a few instances we have been able to detect changes in the spinal course of the corticospinal tract on FLAIR MR images, but the majority of our other cases showed no such changes Several authors have emphasized prolonged motor evoked potentials and conspicuous precentral atrophy on MRI (see Kuipers-Upmeijer et al) The spinal uid and CK level are normal and the EMG reveals no indications of neurogenic denervation unless the spasticity is simply the initial feature of ALS Pathologic studies in a limited number of cases have disclosed a relatively stereotyped pattern of reduced numbers of Betz cells in the frontal and prefrontal motor cortex, degeneration of the corticospinal tracts, and preservation of motor neurons in the spinal cord and brainstem (Beal and Richardson, Fisher, Pringle et al) The corticospinal tract lesions are identical to those in typical ALS, described further on.

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