Fine Hand Movements Research Articles

Effect of Iron-Deficiency Anemia on Cognitive Skills and Neuromaturation in Infancy and Childhood

Iron-deficiency anemia in infancy has been consistently shown to negatively influence performance in tests of psychomotor development. In most studies of short-term follow-up, lower scores did not improve with iron therapy, despite complete hematologic replenishment.The negative impact on psychomotor development of iron-deficiency anemia (IDA) in infancy has been well documented in more than a dozen studies during the last two decades. Two studies will be presented here to further support this assertion. Additionally, we will present some data referring to longer follow-up at 5 and 10 years as well as data concerning recent descriptions of the neurologic derangements that may underlie these behavioral effects.To evaluate whether these deficits may revert after long-term observation, a cohort of infants was re-evaluated at 5 and 10 years of age. Two studies have examined children aged 5 years who had anemia as infants using comparable tools of cognitive development showing persisting and consistent important disadvantages in those who were formerly anemic. These tests were better predictors of future achievement than psychomotor scores. These children were again examined at 10 years and showed lower school achievement and poorer fine-hand movements. Studies of neurologic maturation in a new cohort of infants aged 6 months included auditory brain stem responses and naptime 18-lead sleep studies. The central conduction time of the auditory brain stem responses was slower at 6, 12, and 18 months and at 4 years, despite iron therapy beginning at 6 months. During the sleep-wake-fulness cycle, heart-rate variability—a developmental expression of the autonomic nervous system—was less mature in anemic infants. The proposed mechanisms are altered auditory-nerve and vagal-nerve myelination, respectively, as iron is required for normal myelin synthesis.

Speech and motor disturbances in Rett syndrome.

Rett syndrome is a severe, genetically determined disease of early childhood which produces a defined clinical phenotype in girls. The main clinical manifestations include lesions affecting speech functions, involving both expressive and receptive speech, as well as motor functions, producing apraxia of the arms and profound abnormalities of gait in the form of ataxia-apraxia. Most investigators note that patients have variability in the severity of derangement to large motor acts and in the damage to fine hand movements and speech functions. The aims of the present work were to study disturbances of speech and motor functions over 2-5 years in 50 girls aged 12 months to 14 years with Rett syndrome and to analyze the correlations between these disturbances. The results of comparing clinical data and EEG traces supported the stepwise involvement of frontal and parietal-temporal cortical structures in the pathological process. The ability to organize speech and motor activity is affected first, with subsequent development of lesions to gnostic functions, which are in turn followed by derangement of subcortical structures and the cerebellum and later by damage to structures in the spinal cord. A clear correlation was found between the severity of lesions to motor and speech functions and neurophysiological data: the higher the level of preservation of elements of speech and motor functions, the smaller were the contributions of theta activity and the greater the contributions of alpha and beta activities to the EEG. The possible pathogenetic mechanisms underlying the motor and speech disturbances in Rett syndrome are discussed.

Functional switch between motor tracts in the presence of the mAb IN-1 in the adult rat

Fine finger and hand movements in humans, monkeys, and rats are under the direct control of the corticospinal tract (CST). CST lesions lead to severe, long-term deficits of precision movements. We transected completely both CSTs in adult rats and treated the animals for 2 weeks with an antibody that neutralized the central nervous system neurite growth inhibitory protein Nogo-A (mAb IN-1). Anatomical studies of the rubrospinal tracts showed that the number of collaterals innervating the cervical spinal cord doubled in the mAb IN-1- but not in the control antibody-treated animals. Precision movements of the forelimb and fingers were severely impaired in the controls, but almost completely recovered in the mAb IN-1-treated rats. Low threshold microstimulation of the motor cortex induced a rapid forelimb electromyography response that was mediated by the red nucleus in the mAb IN-1 animals but not in the controls. These findings demonstrate an unexpectedly high capacity of the adult central nervous system motor system to sprout and reorganize in a targeted and functionally meaningful way.

Critical decline in fine motor hand movements in human aging.

Slowing of motor movements in human aging is a well-known occurrence, but its biologic basis is poorly understood. Reliable quantitation may refine observations of this phenomenon to better aid research on this entity. A panel equipped with timing sensors under computer control was used to measure upper extremity movement times in two groups of healthy individuals: adults younger than 60 years of age (n = 56; range, 18-58 years) and adults older than 60 years of age (n = 38; range, 61-94 years). Fine motor performance was better in the dominant hand (p = 0.0007) regardless of age. Adult and aged groups differed on two basic timing measures, which reflect coarse motor and fine motor performance (p < 0.0001). There were no gender differences on either measure. There was a strong effect of task difficulty with age on coarse motor (p < 0.01) and fine motor (p < 0.0001) measures. The fine motor measure of hand performance in healthy individuals correlated in a nonlinear fashion with age for more difficult tasks (r2 = 0.63) but showed a simple linear relation for less-demanding tasks (r2 = 0.5). This technique sensitively detects age-related motor performance decline in humans. There may be a critical period in late midlife when fine motor performance decline either begins or abruptly worsens.

A primate genesis model of focal dystonia and repetitive strain injury: I. Learning-induced dedifferentiation of the representation of the hand in the primary somatosensory cortex in adult monkeys.

In this study we tested a neuroplasticity/learning origins hypothesis for repetitive strain injuries (RSIs), including occupationally induced focal dystonia. Repetitive movements produced in a specific form and in an appropriate behavioral context cause a degradation of the sensory feedback information controlling fine motor movements, resulting in the "learned" genesis of RSIs. Two adult New World owl monkeys were trained at a behavioral task that required them to maintain an attended grasp on a hand grip that repetitively and rapidly (20 msec) opened and closed over short distances. The monkeys completed 300 behavioral trials per day (1,100 to 3,000 movement events) with an accuracy of 80 to 90%. A movement control disorder was recorded in both monkeys. Training was continued until the performance accuracy dropped to below 50%. We subsequently conducted an electrophysiologic mapping study of the representations of the hand within the primary somatosensory (SI) cortical zone. The hand representation in the true primary somatosensory cortical field, SI area 3b, was found to be markedly degraded in these monkeys, as characterized by (1) a dedifferentiation of cortical representations of the skin of the hand manifested by receptive fields that were 10 to 20 times larger than normal, (2) the emergence of many receptive fields that covered the entire glabrous surface of individual digits or that extended across the surfaces of two or more digits, (3) a breakdown of the normally sharply segregated area 3b representations of volar glabrous and dorsal hairy skin of the hand, and (4) a breakdown of the local shifted-overlap receptive field topography of area 3b, with many digital receptive fields overlapping the fields of neurons sampled in cortical penetrations up to more than four times farther apart than normal. Thus, rapid, repetitive, highly stereotypic movements applied in a learning context can actively degrade cortical representations of sensory information guiding fine motor hand movements. This cortical plasticity/learning-based dedifferentiation of sensory feedback information from the hand contributes to the genesis of occupationally derived repetitive strain injuries, including focal dystonia of the hand. Successful treatment of patients with RSI will plausibly require learning-based restoration of differentiated representations of sensory feedback information from the hand.

Mirror use by African Grey parrots (Psittacus erithacus).

Mirror use by African Grey parrots (Psittacus erithacus).

Extensive cervical intradural and intramedullary lipoma and spina bifida occulta of C1: a case report

A 17-year-old boy presented with a 1-year history of progressive gait difficulties and slowing of fine hand movements. On neurological examination there was tetraspasticity, bilateral pes equinovarus and a decreased position sense in the feet. CT and MRI scan of the cervical spine demonstrated a spina bifida occulta of C1, an extensive intradural lipoma from the foramen magnum to C4 with a small intramedullary portion at C3, and a distal syringomyelia reaching down to D12. After excision of the extramedullary portion of the lipoma, there was a marked improvement of the gait and a reduction of the spasticity.

The effect of fasciculus cuneatus lesions on finger positioning and long-latency reflexes in monkeys.

Previous studies have reported abnormalities in fine hand and finger movements following interruption of the fasciculus cuneatus (FC) in primates. We report here that many of these deficits could be caused by an inability to actively regulate the position of the finger. Three macaques were trained to maintain the index finger in one position against constant or changing loads. Periodically, torque pulses were used to elicit reflexes in finger muscles. Following unilateral FC lesions, the monkeys failed to adjust finger position during the trials, and the normal M2 long-latency response was absent in the finger muscles. Performance on the task was impaired only in monkeys with complete lesions that included the deep ventral portion of the FC. These results suggest that afferent fibers in the FC regulate finger position, and do so partly through reflexive mechanisms. When the FC is interrupted, the inability to control finger position disturbs fine motor activities.

The prognosis of convulsions during childhood shigellosis

We examined the long-term outcome in 111 children who had convulsions during shigellosis and were followed for 3-18 years after the incident. No deaths or persistent motor deficits occurred as sequellae. Poor coordination of fine hand movements were noted in 3.3% of the 92 children who had no pre-existing neurological abnormality. Only 1 child developed epilepsy by the age of 8 years. Of the children 15.7% had recurrent febrile seizures. The only risk factor identified for febrile seizures following convulsions in shigellosis was a previous history (P less than 0.01). These observations suggest that convulsions in shigellosis have a favourable prognosis, and do not necessitate long-term follow up.

Comparison of deficits induced by a local injection of muscimol into the first somatosensory cortex (SI) or motor cortex on the fine hand movements of a trained monkey

Comparison of deficits induced by a local injection of muscimol into the first somatosensory cortex (SI) or motor cortex on the fine hand movements of a trained monkey

Fetal deafferentation: The ontogenesis of movement in the absence of peripheral sensory feedback

Three monkeys were deprived of sensation in their forelimbs by sectioning dorsal roots C2-T3 bilaterally prior to delivery. The infants were active and used their limbs in proper sequence during walking. They did not, however, use their hands to climb or pick up objects. It was concluded that the fine hand movements seen in monkeys deafferented during adolescence are elaborated on the basis of engrams laid down prior to surgery.

Paralysis of the ulnar nerve and management of its deformity.

p ARALYSIS Of the ulnar nerve has been more frequent and unfortunately the results of suture of this nerve have given less gratifying results than in any other peripheral nerve. Reasons for this are: (1) the ulnar is a mixed motor and sensory nerve carrying different types of nerve fibers, (~) distal innervation is to small highly specialized muscles for the finer movements of the hand, (3) another reason may be the poor blood supply of the nerve which may be further impaired by anterior transplantat ion of the nerve. The functional return of a useful hand should be the objective when confronted with an ulnar nerve paralysis. This may be obtained by neurorrhaphy or by a combination of primary nerve repair followed by tendon transfers for deficient regeneration. In either case we must preserve the parts of the hand that are essential for function. An innervated, but stiff hand is useless. Steps must be taken to preserve muscles, joints and soft tissues in a state of mobility. I t seems to the writer that mechanical splintage of paralyzed joints must follow more closely the anatomical and physiological characteristics of a part. The prevention of muscle stretching is important , but the joint structures on which the muscle acts must also be considered; namely, the ligaments, joint capsules and soft tissues. For example, t ight skin about a joint can vitiate completely normal nerve-muscle-joint mechanism. Paralysis of the ulnar nerve sparing the nerves to the flexor digitorum profundus muscle presents a deformity of the hand that is not seen when the lesion is above the elbow. Phylogenetically, the muscles innervated by the ulnar nerve arc oldest and more highly co-ordinated than those supplied by other peripheral nerves. This nerve is peculiar by supplying muscles at different levels in the extremity, but which co-ordinate for fine hand movement involving identical joints. An active flexor digitorum profundus muscle sets in motion the platform of origin of the lumbrical muscles. The latter, however, have their insertion upon the dorsal expansion of the metaearpophalangeal joint. Paralysis of the ulnar nerve above the elbow, producing a flail state of all the muscles supplied by this nerve, causes a minimal deformity of the hand. However, a lesion below the elbow sparing the innervation of the