Meaning : Be careful to not waste your kindness on ungrateful people who will simply abuse your generosity. Translation: In bad times, a good face. Meaning : Hold your head high even when the going gets tough. Translation : He who wants to catch fish must get his arse wet. Better to be the best at something less ambitious than average at something more impressive.
Translation : The old Moor will never be a good Christian. Translation: He who went to Seville, lost his seat. Move your feet, lose your seat.
Meaning : Things go to those who need them; only the squeaky wheel gets greased. Translation : Shoemaker, to your shoes! Meaning : Keep to what you know, and mind your own business. Translation : A cat with gloves does not catch mice. Meaning : Be prepared to get your hands dirty if you want to get the job done. Translation : Keep your accounts clear and your chocolate thick. Translation : To day old bread, a three-week hunger.
The phylogenetic meaning of this reflex also remains unclear [ 9 , 10 ]. It is interesting that, in spite of the great difference in the motor behavior, there is a close interrelationship between these primitive reflexes in the responses: the palmar grasp reflex inhibits the Moro reflex [ 12 , 14 — 17 ].
This paper mainly concerns the clinical significance and neural mechanism of the grasp reflex and the Moro reflex and also attempts to discuss the meaning of these reflexes based on comparison of the responses in human infants with those in monkey infants and the hierarchical interrelation of the responses of the primitive reflexes.
To elicit the palmar grasp reflex, the examiner inserts his or her index finger into the palm of the infant from the ulnar side and applies light pressure to the palm, with the infant lying on a flat surface in the symmetrical supine position while awake [ 18 — 20 ].
Tactile without pressure and nociceptive stimulation of the palm are both inadequate. The latter occurs as a reaction to the proprioceptive stimulation of the tendons of the finger muscles due to slight traction subsequent to the application of pressure to the palm [ 21 , 22 ]. The plantar grasp reflex is elicited by pressing a thumb against the sole of a foot just behind the toes [ 6 , 18 , 23 ]. The state and position are the same as for eliciting the palmar grasp reflex.
The response of the reflex consists of flexion and adduction of all the toes. Milani-Comparetti and Gidoni [ 24 ] devised another method for eliciting the plantar grasp reflex. They tested for the presence of the reflex by placing the infant in a supported standing position, stimulating the soles of the feet by floor contact, looking for plantar flexion of the toes. Determination of whether the response of the hands and feet is a true reflex or a voluntary grasping movement can be difficult in older infants.
The grasp reflexes of the hands and feet in normal term infants have been studied by several authors. Their results were fairly consistent regarding the times of the appearance and disappearance of the reflexes.
The palmar grasp reflex and the plantar grasp reflex can be elicited in all infants during the first 3 and 6 months of age, respectively. Thereafter they decrease along with the intensity of the responses, usually disappearing by 6 and 12 months of age, respectively [ 6 , 7 , 25 — 27 ]. The disappearance of the reflexes is significantly related to the commencement of the voluntary use of hands or standing [ 28 , 29 ].
In contrast to the studies involving term infants, those involving preterm infants have been few. Allen and Capute [ 1 ] examined 47 infants and concluded that the intensity of the primitive reflexes including the grasp reflexes of the hands and feet in the preterm infant at term 40 weeks of PCA was similar to that in full-term newborns reported in the literature. We analyzed the data for infants term and preterm who were later confirmed to be normal on follow-up examination between ages 3 to 9 years [ 6 ].
The primitive reflex responses of preterm infants were compared with those of term infants, according to corrected age as to expected birth date. No difference was evident in the changes in responses including that of the plantar grasp reflex between term and preterm infant groups throughout the first year of life. In general, a primitive reflex in infants is regarded as abnormal when it is absent or diminished during the period it should be actively elicitable or lasts beyond the normal age limit for its disappearance.
An exaggerated reflex can also be abnormal. The response of the palmar grasp reflex may be less intense during the first and second days after birth [ 18 ]. The absence of this reflex usually reflects peripheral i. However, lesions of the upper brain structures also can affect the response. The response may be increased and retained longer, compared with that in normal infants, on the affected side s of the upper limb s in infants with spastic hemiplegia or quadriplegia, whereas it is very weak in infants with cerebral palsy CP of the athetoid type [ 26 , 27 , 32 ].
The clinical value of the plantar grasp reflex in infants has been investigated in more detail than that of the palmar grasp reflex.
In , Brain and Curran [ 33 ] reported two cases showing no response at the age of 6 months who both suffered from bilateral marked spasticity and one case showing a vigorous response at the age of 2. They discovered that up to age 20 years, the response was present in 25 of 42 patients and, after age 20 years, in 3 of We analyzed infants term and preterm whose plantar grasp reflex was examined before 1 year of age [ 5 ].
Their diagnoses were confirmed by follow-up examinations and comprised normality in , CP in 78, and mental retardation MR in We obtained several results: the reflex reactivity in infants with CP of the spastic type was significantly reduced; infants with CP of the athetoid type exhibited an extremely strong retention of the reflex; infants with MR also exhibited a tendency for prolonged retention of the reflex; the reflex profile in infants with CP of the athetoid type with spasticity, or of the ataxic type, was not different from that in normal control subjects.
Other authors also reported the characteristics of the plantar grasp reflex in children with neurodevelopmental abnormalities of various types, and their results were well consistent with ours [ 26 , 27 , 34 ].
A reduced or negative plantar grasp reflex during early infancy can be a sensitive indicator of later development of spasticity. Of infants whose plantar grasp reflex had been examined before 1 year of age, we analyzed the neurodevelopmental outcome in 47 infants exhibiting a negative response during the first 6 months of age and in 46 infants exhibiting a significantly reduced response at ages 1 to 4 months [ 6 ].
The diagnoses comprised CP in 75, MR in 7, borderline intelligence in 2, motor delay in 1, and normality in 8. Of the 75 cases with CP, 69 had the spastic type and 4 the athetoid type with spasticity. The total number of patients with CP of the spastic type or the mixed type with spasticity among the entire infants in this series was , and 73 of these patients with CP with spasticity In the remaining 34 infants with CP with spasticity who exhibited a normal response during the corresponding period, the extent of motor disturbance was significantly milder [ 35 ].
A high concordance between the side of an abnormal plantar grasp reflex during infancy and the laterality of the disturbance of motor function in children with CP of the spastic type was demonstrated [ 36 ]. The side affected, or more affected, in motor function was in accordance with the side that exhibited a diminished or more diminished response in most subjects with spastic hemiplegia, diplegia, and quadriplegia.
Because anencephalic infants demonstrate a positive grasp reflex in both the hands and feet, the cerebral hemispheres are apparently not necessary for the reflexes [ 37 — 39 ].
Shahani et al. This short latency excludes the long cerebral reflex arcs and puts this grasp reflex in the category of segmental reflexes mediated at the level of the spinal cord. The spinal reflex center, however, is controlled by a higher brain mechanism. The grasp reflexes can be elicited in neonates and early infants as a result of insufficient control of the spinal mechanism by the immature brain, but the reflexes gradually disappear with age, due to the increased inhibition accompanying brain maturation [ 23 , 41 ].
Adult patients with lesions in the frontal lobes sometimes exhibit a grasp reflex of the hands and feet [ 23 , 33 , 37 , 41 — 45 ].
Such reappearance of these reflexes in adults is attributed to the release of the spinal reflex center from the disturbed higher brain mechanism, suggesting that these reflexes are only inhibited, and not lost, after the infantile period. Many attempts have been made to determine the pathological site of the grasp reflexes by means of clinical observation or animal experiments [ 37 , 46 — 48 ].
In , Adie and Critchley [ 37 ] analyzed 13 patients with a tumor or vascular lesion in a frontal lobe who exhibited a palmar grasp reflex on the side opposite to that of the diseased frontal lobe.
They confirmed that the palmar grasp reflex was most evident when pyramidal signs were absent, and thus they concluded that the lesion responsible for the reflex was extrapyramidal. In , Goldstein [ 41 ] described that a lesion involving the medial aspect of a frontal lobe seemed to be especially prone to produce the plantar grasp reflex on the opposite side. More recent studies have implicated lesions of the medial or lateral frontal cortex anterior to the primary motor area, that is, the supplementary motor area SMA , premotor cortex, and cingulate motor cortex, as the etiology of the palmar grasp reflex [ 23 , 45 , 48 , 49 ].
These findings indicate that nonprimary motor areas comprise substantial portions of the brain that exert inhibitory control over the spinal reflex mechanism underlying the grasp reflexes and that the destruction of these structures will release the inhibitory control and thus lead to the reappearance of the reflexes.
Nonprimary motor areas play important roles in the planning, preparation, initiation, and execution of motor behavior [ 50 — 55 ]. These areas contain corticospinal neurons and thereby a somatotopically arranged map of the body [ 54 , 56 — 58 ]. However, the cortical projections from these areas to the spinal cord do not necessarily have a direct influence on spinal motor neurons.
The majority of the neurons terminate in the intermediate zone in the spinal cord and connect with interneurons [ 53 , 56 , 59 , 60 ]. The essential roles of nonprimary motor areas in the spinal cord are thought to be in the preparation and modulation of the spinal circuitry through interneurons rather than the generation of movements that require a direct command to the spinal motor neurons [ 52 , 53 , 60 , 61 ].
On the other hand, because interneurons are substantially related to the modulation of spinal reflexes [ 52 , 57 ], the descending inhibitory control of the grasp reflexes by nonprimary motor areas may also occur through spinal interneurons. As brain maturation proceeds, increasing control of the spinal circuit by the nonprimary motor areas will replace the simple reflex grasping during early infancy, with more regulatory and adaptive voluntary grasping in older infants.
However, the proportion of patients with a lesion of a nonprimary motor area in whom a grasp reflex can be elicited is not necessarily high. On the other hand, a minority of patients with a deep lesion including the basal ganglia without frontal cortical damage were reported to exhibit a positive palmar grasp reflex [ 44 ], and the extension of an SMA lesion into more lateral regions of area 6 may increase the strength of the grasp reflex [ 48 ].
These observations seem to indicate that the inhibitory stimuli from upper brain structures travel via multiple routes [ 44 ], and the extent of the release of control depends not only on the specificity of the location but also on the extent and severity of the lesions. Clinical studies have revealed that some patients with a frontal lesion exhibit a grasp reflex of the hands or feet, or both [ 33 , 41 , 43 ].
This finding suggests that different sites are specific to each of the grasp reflexes of the hands and feet within the nonprimary motor cortex. As demonstrated, each nonprimary motor area retains some degree of a somatotopically arranged map of the body that represents peripheral innervation, which is dominated by descending pathways from the area through connections to different levels of the spinal cord [ 54 , 56 — 58 ].
We speculate that the grasp reflexes of the hands and feet may be elicited according to the specific location of each lesion corresponding to the fingers or toes on the map in nonprimary motor areas.
In normal circumstances, higher brain centers control the spinal mechanism that regulates the coordination among agonists, antagonists, and synergists in an adaptable manner by means of reciprocal innervation. In children with spastic type CP, however, deviation in terms of reciprocal innervation caused by damage to the pyramidal tract leads to excess cocontraction at proximal joints, whereas deviation leads to excess reciprocal inhibition through spastic antagonists at distal joints, inducing weakness of the agonists [ 62 ].
A diminished or negative plantar grasp reflex may be caused by weak toe flexors, as induced by excessive reciprocal inhibition of the flexors through the predominance of extensors over flexors in tonus in a lower limb in these children. They also exhibit the predominance of finger flexors over extensors in their upper limbs, which may cause a facilitated palmar grasp reflex on the affected side s in spastic hemiplegia and quadriplegia.
On the other hand, in children with CP of the athetoid type, the deviation of reciprocal innervation always leads to excess reciprocal inhibition. Any attempt at movement produces excessive relaxation of the antagonists, inducing an extreme range of movements [ 62 ]. Although the released control of the spinal reflex mechanism because of a lesion in the basal ganglia seems to be the most likely cause of facilitation of the plantar grasp reflex in these children, the excessive relaxation of toe extensors, in response to the toe flexion at the moment of elicitation of the reflex, may be another factor causing an exaggerated response.
Children with athetosis generally exhibit decreased tonus of finger muscles, especially of flexors, which causes a weak grasp and the release of objects too easily [ 62 ]. The relative predominance of finger extensors over flexors, in addition to the specific weakness of the finger muscles, may be a factor causing the diminished palmar grasp reflex in these children.
In infants, the maturation of cortical connections overrides the generators of primitive reflexes in the spinal cord and brain stem with age and eventually leads to the disappearance of the primitive reflexes and the emergence of righting and equilibrium reactions [ 34 , 63 ]. The disappearance and emergence of these reflex mechanisms were demonstrated to be chronologically related to the attainment of motor milestones in normal children [ 24 ].
In children with MR, however, the process of evolution of these reflex mechanisms is prolonged, in accordance with the retardation of maturation in brain function, resulting in retention of primitive reflexes and the delayed attainment of motor milestones [ 24 , 29 , 34 , 64 ]. Later a variety of methods for eliciting the reflex were devised including hitting on the table surface, warm or cold application to the chest or stomach, and a tap on the abdomen [ 10 , 11 ].
Infants should be tested while they are awake, but not crying [ 18 ]. There is no dorsiflexion of the neck with this technique [ 18 ]. The initial phase of the response comprises abduction of the upper limbs at the shoulders and extension of the forearms at the elbows, with slight extension of the spine and retraction of the head.
There is sometimes a slight tremor or clonus-like rhythmic movements of the limbs. Subsequently the arms adduct at the shoulders and the forearms flex at the elbows: the upper limbs describe an arc-like movement, bringing the hands in front of the body, which finally return to the original position [ 10 , 11 , 18 ]. The responses of the lower limbs are usually eliminated from the evaluation, because they show wide variability among the normal population [ 11 , 19 , 20 ].
With this reflex, habituation develops only on an experimental basis with intensively repetitive trials, that is, not in the clinical setting [ 17 , 66 ]. No significant difference in the response has been reported at birth or through the first 5 months of age between the term cephalic-presenting and breech-presenting infant groups [ 67 ].
The study of the Moro reflex in normal term infants has been undertaken by many authors. The results obtained with the head drop method are well consistent. The reflex can be elicited in all infants during the first 12 weeks of age. After the neonatal period, however, the response becomes increasingly less typical with age, eventually consisting only of abduction and extension of the upper limbs.
The reflex usually disappears by 6 months of age [ 11 , 31 , 68 — 70 ]. Several authors compared the Moro reflex in preterm infants tested at 40 weeks PCA or at 4 months of corrected age with that in term infants. Although none of the studies confirmed the outcome in the subjects, there is a general agreement as to the similarity in the response between the two groups, especially when only infants with no or low perinatal risk factors are compared [ 1 , 71 — 75 ].
Based on the findings in normal infants, the absence or diminution of the Moro reflex within 2 to 3 months of age and the persistence of the response beyond 6 months of age can be regarded as abnormal. The absence of the response during the neonatal period and early infancy is of especial clinical significance and may indicate a compromised condition or disorder including birth injury, severe birth asphyxia, intracranial hemorrhage, infection, brain malformation, general muscular weakness of any cause, and CP of the spastic type [ 10 , 31 , 69 , 76 , 77 ].
On the other hand, a hyperactive response of the reflex is a common feature of neonatal withdrawal from maternal drug abuse including volatile substances, heroin, and opioids [ 78 — 80 ]. An exaggerated response may also be detected in infants with a severe bilateral intrauterine disturbance such as hydranencephaly [ 31 ]. Asymmetry of the response is usually a sign of local injury. Damage to a peripheral nerve or cervical cord or a fracture of the clavicle may inhibit the reflex on the affected side.
However, it should be noted that Dubowitz [ 14 ] demonstrated an asymmetrical response in normal infants. Their responses appeared to be related to the clenching of one fist during the procedure, and he considered that this might be caused by inhibition of the response on one side due to contraction of the finger flexors. Because Reiners et al. It is also sometimes observed in children with a severe brain malformation or with CP of the spastic type [ 31 , 69 ].
Katona [ 17 ] reported that the Moro reflex could be elicited in anencephalic newborns with a nervous system that had developed only to the rostral level of the pons. In a study involving analysis of the relationship between the morphological structures of the rudimentary brain and primitive reflexes in six anencephalic newborns, Hanabusa [ 39 ] found that the Moro reflex could be elicited only when the vestibular nuclei were preserved.
This finding indicates that the reflex is principally mediated by the vestibular nuclei. These latencies are much longer than those of the spinal reflexes, clearly indicating that the reflex is mediated in the brain stem, not at the level of the spinal cord [ 83 , 84 ].
Thus, the center of the Moro reflex seems to be in the lower region of the pons to the medulla. The origin of afferent pathways for the Moro reflex, whether it is primarily vestibular, proprioceptive, or exteroceptive, has been a main subject of discussion. The head drop, the most common way of eliciting the reflex, stimulates both the vestibular system and the proprioceptive receptors in the neck.
Prechtl [ 12 ] also demonstrated that sudden raising or dropping of the infants, whose head, neck, and trunk were fixed in a plaster cast, could elicit the response.
Bloomfield et al. These findings support the view that this reflex is principally mediated by the vestibular system. In contrast to the grasp reflex, the Moro reflex has not been observed in a fetus, which is also in agreement with its vestibular origin, because fetuses are protected from acceleration or shaking in intrauterine life [ 68 , 86 ]. On the other hand, Parmelee Jr.
Prechtl [ 12 ] described an infant with bilateral absence of the inner ears who had exhibited a normal Moro response to a head drop, which was reported by Karlsson in an address to a study group in Oxford. These observations suggest that the proprioceptive inputs from the neck also contribute to elicitation of the reflex. There are direct and indirect, via the cervical cord, ascending pathways that originate in the proprioceptive receptors in the neck and connect with vestibular nuclei.
These pathways originally send signals to the brain stem to regulate the neck righting [ 57 ]. The signals generated by the head drop may travel via these routes to reach and activate the reflex mechanism in the brain stem. The head drop method is most effective, because it produces a large number of ascending signals to the target through the two pathways and thereby induces a high level of neural excitation that acts on the reflex center.
Besides the primary somatosensory afferents, there is a path taken by nociceptor axons that reaches the pontine reticular formation, which has close interconnections with vestibular nuclei [ 87 — 89 ]. The nociceptive signals may travel via this pathway toward the reflex center in the brain stem. Armored Core Wiki Explore. Explore Wikis Community Central. Register Don't have an account? Dan Moro. Edit source History Talk 0.
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