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AIDS TO THE EXAMINATION OF THE PERIPHERAL NERVOUS SYSTEM London, Balliere Tindall/Saunders, 1986 ` ASANUMA H: Cerebral cortical control of movement Physiologist 16:143, 1973 ASANUMA H: The pyramidal tract, in Brooks VB (ed): Handbook of Physiology Sec 1: The Nervous System Vol 2: Motor Control, Part 2 Bethesda, MD, American Physiological Society, 1981, pp 702 733 ASH J, GEORGOPOULOS AP: Mechanisms of motor control, in Asbury AK, McKhann GM, McDonald WI, et al (eds): Diseases of the Nervous System, 3rd ed Cambridge, Cambridge University Press, 2002, chap 31, pp 447 460 AY H, BUONANNO FS, PRICE BH, et al: Sensory alien hand syndrome J Neurol Neurosurg Psychiatry 65:366, 1998 BRODAL P: The Central Nervous System: Structure and Function, 5th ed New York, Oxford University Press, 1992 BROWN P: Pathophysiology of spasticity J Neurol Neurosurg Psychiatry 57:773, 1994 BUCY PC, KEPLINGER JE, SIQUEIRA EB: Destruction of the pyramidal tract in man J Neurosurg 21:385, 1964 BURKE D, LANCE JW: Myotatic unit and its disorders, in Asbury AK, McKhann GM, McDonald WI (eds): Diseases of the Nervous System: Clinical Neurobiology, 2nd ed Philadelphia, Saunders, chap 20, pp 270 284 DAVIDOFF RA: Antispasticity drugs: Mechanisms of action Ann Neurol 17:107, 1985 DAVIDOFF RA: Skeletal muscle tone and the misunderstood stretch re ex Neurology 42:951, 1992 DENNY-BROWN D: The Cerebral Control of Movement Spring eld, IL, Charles C Thomas, 1966 DENNY-BROWN D: The nature of apraxia J Nerv Ment Dis 12:9, 1958 EVARTS EV, SHINODA Y, WISE SP: Neurophysiological Approaches to Higher Brain Functions New York, Wiley, 1984 FAGLIONI PR, BASSO A: Historical perspectives on neuroanatomical correlates of limb apraxia, in Roy EA (ed): Neuropsychological Studies of Apraxia and Related Disorders Amsterdam, North Holland, 1985, pp 3 44 FEINBERG TE, SCHINDLER RJ, FLANAGAN NG, HABER LD: Two alien hand syndromes Neurology 42:19, 1992 FULTON JF: Physiology of the Nervous System New York, Oxford University Press, 1938, chap 20 FULTON JF, KELLER AD: The Sign of Babinski A Study in the Evolution of Cortical Dominance in Primates Charles C Thomas, Spring eld, 1932 GESCHWIND N: The apraxias: Neural mechanisms of disorders of learned movement Am Sci 63:188, 1975 GILMAN S, MARCO LA: Effects of medullary pyramidotomy in the monkey Brain 94:495, 515, 1971 HALLETT M, SHAHANI BT, YOUNG RR: EMG analysis of stereotyped voluntary movements in man J Neurol Neurosurg Psychiatry 38:1154, 1975 HENNEMAN E: Organization of the spinal cord and its re exes, in Mountcastle VB (ed): Medical Physiology, 14th ed Vol 1 St Louis, Mosby, 1980, pp 762 786 IWATSUBO T, KUZUHARA S, KANEMITSU A, et al: Corticofugal projections to the motor nuclei of the brain stem and spinal cord in humans Neurology 40:309, 1990 KERTESZ A, FERRO JM, SHEWAN CM: Apraxia and aphasia: The functional anatomical basis for their dissociation Neurology 34:40, 1984 LANCE JW: The control of muscle tone, re exes and movement: Robert Wartenburg Lecture Neurology 30:1303, 1980 LAPLANE D, TALAIRACH J, MEININGER V, et al: Motor consequences of motor area ablations in man J Neurol Sci 31:29, 1977 LASSEK AM: The Pyramidal Tract Spring eld, IL, Charles C Thomas, 1954 LAWRENCE DG, KUYPERS HGJM: The functional organization of the motor system in the monkey Brain 91:1, 15, 1968 LIEPMANN H: Das Krankheitsbild der Apraxie (motorische Asymbolie auf Grund eines Falles von einseitiger Apraxie) Monatsschr Psychiatry Neurol 8:15, 102, 182, 1900 LORENTE DE NO R: Cerebral cortex: Architecture, intracortical connections, motor projections, in Fulton JF (ed): Physiology of the Nervous System, 3rd ed New York, Oxford University Press, 1949, pp 288 330 LURIA AR: The Working Brain: An Introduction to Neuropsychology New York, Basic Books, 1973 MOUNTCASTLE VB: Central nervous mechanisms in sensation, in Mountcastle VB (ed): Medical Physiology, 14th ed Vol 1: Part 5 St Louis, Mosby, 1980, chaps 11 19, pp 327 605 NATHAN PW, SMITH M, DEACON P: Vestibulospinal, reticulospinal and descending propriospinal nerve bers in man Brain 119:1809, 1996 NYBERG-HANSEN R, RINVIK E: Some comments on the pyramidal tract with special reference to its individual variations in man Acta Neurol Scand 39:1, 1963 PANTANO P, FORMISANO R, RICCI M, et al: Prolonged muscular accidity after stroke Morphological and functional brain alterations Brain 118: 1329, 1995 PAUSE M, KUNESCH F, BINKOFSKI F, FREUND H-J: Sensorimotor disturbances in patients with lesions of the parietal cortex Brain 112:1599, 1989.

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motor milestones or with motor skill at a later time Children with cerebral defects tend to exhibit apathy or hyperactivity more often than children without recognizable defects Again, two groups of overactive children can be discerned In one, infants are constitutionally overactive from birth, sleeping less and feeding poorly; by the age of 2 years, the syndrome is obvious In the other group, an inability to sit quietly only becomes apparent at the preschool age (4 to 6 years) Seldom do such children remain in one position for more than a few seconds, even when watching television Attention to any task cannot be sustained, hence the term attention de cit hyperactivity disorder As a rule, there is also an abnormal impulsivity and often an intolerance of all measures of restraint Mild degrees of mental retardation and epilepsy and other disabilities are conjoined in some patients Once the child is in school, the attention de cit becomes more troubling Now these children must sit still, watch and listen to the teacher when she speaks to another child, and not react to distracting stimuli They cannot stay at their desks, take turns in reciting, be quiet, or control their impulsivity The teacher nds it dif cult to discipline them and often insists that the parents seek medical consultation A few affected children are so hyperactive that they cannot attend regular school Their behavior verges on the organic drivenness that has been known to occur in children whose brains have been injured by encephalitis In certain families the disorder is probably inherited (Biederman et al) In about half the patients, the hyperactivity subsides gradually, by puberty or soon thereafter, but in the remainder the symptoms persist in modi ed form into adulthood (Weiss et al) It has also become clear that a group of children exist who have dif culty sustaining concentration but do not manifest hyperactivity or behaviors that betray the attention de cit It is presumed that they share a similar core problem with hyperkinetic children, and it has been observed that they may be helped in studying and school performance by the same stimulant drugs that are used for the treatment of more overt ADHD For a number of years there was a tendency to consider children with the hyperkinetic syndrome as having minimal brain disease Soft neurologic signs such as right-left confusion, mirror movements, minimal choreic instability of the hands, awkwardness, nger agnosia, tremor, and borderline hyperre exia were said to be more frequent among them These signs, however, are seen so often in normal children that their attribution to disease is invalid Schain and others therefore substituted the term minimal brain dysfunction, which is no more accurate and simply restates the problem Lacking altogether are accurate clinicoanatomic and clinicopathologic correlative data Some morphologic and physiologic data are available In an MRI study of the brains of 10 children with hyperactivity attention de cit disorder, Hynd and colleagues found the width of the right frontal lobe to be smaller than normal; also fairly consistently, there was smallness of the dorsolateral, cingulate, and striatal regions Unlike dyslexics, in whom the planum temporale tends to be equal in the two hemispheres, the left planum was larger in the attention de cit cases, just as it is in normals Also, functional imaging studies have suggested that the inability of these children to block impulsive reactions and the improvement that is seen with methylphenidate are accompanied by changes in the striatum One would expect the prefrontal cortex to be implicated in such a disinhibitory syndrome but data from brain mapping in children with ADHD have been very complex and dif cult to interpret Another approach to understanding the process has been to study a strain of mice that have been genetically altered to eliminate a dopamine transporter.

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