Primitive reflexes and therir pathway . pptxtx

Primitive reflex pathway

1. PRIMITIVE REFLEX PATHWAY

2. Primitive reflexes are involuntary motor responses originating in the brainstem present after birth in early child development that facilitate survival These central nervous system motor responses are eventually inhibited by 4 to 6 months of age as the brain matures and replaces them with voluntary motor activities but may return with the presence of neurological disease, especially those affecting the frontal lobes.

3. Initially lower centers such as spinal cord control these movements but later higher centers like midbrain and cortex take control over them and dominate lower ones thus integrating them for various voluntary functional task Disappearance of certain primitive reflex does not mean they are abolished but means that they have been taken over by stronger reflexes at higher level in the CNS

4. These primitive reflexes are classified according to the level at which they are controlled . Accordingly ,we have four levels at which these reflexes are regulated Spinal cord Brain stem Mid brain Cortex There is a fifth category called automatic reflexes eg:Moro’s reflex ,Landau reflex,Parachute reflex

5. What is A Primitive Reflex? ‰ Automatic, repetitive specific movement patterns ‰ Initiated and controlled by the brainstem ‰ Emerge in utero - integrated within 1st year of life ‰ Inhibited by higher brain areas and then integrated within the nervous system ‰ Our first sensory motor experiences ‰ Retained with atypical neurology, poorly developed motor systems ‰ Reappear with trauma, dementia, or brain injury

6. Primitive Reflexes Have Purposes ‰ Assist in birth: work with mother’s reflexes for vaginal birth ‰ Survival: Automatic subconscious responses to changes or stimuli within or outside our bodies ‰Maintain homeostasis: heart rate, breathing, digestion ‰ Automatic actions: swallowing, sneezing, coughing, and vomiting ‰ Serve as early motor experiences

7. Developmental Model Related to Reflexes ‰As a child reaches their developmental milestones, neurological information is sent to the brain to inhibit primitive brain activity. ‰PRs become “stored neurological codes” once their purpose has been fulfilled, and higher brain centers are formed and myelinated. ‰Postural Reflexes are added to the capacities of the CNS as the brain matures.

8. Reflexes and Human Performance ‰ Reflexes are part of our “neurological code” ‰ Utilizing reflexes reinforce the code and act to write more advance codes ‰ As primitive reflexes mature, the brain evolves to cortically control complex skills ‰ Coordination, posture, emotional wellbeing, sensory processing, social engagement, critical thinking, and functional vision skills all evolved from the neurological foundations of our primitive nervous system

9. PRs and BI ‰ PRs can re-emerge with brain trauma and neurodegeneration ‰ Especially with damage to the CNS rostral to the spinal cord ‰ The parts of the CNS that regulate vital functions form first ‰ What is required most for survival forms first (sequential CNS maturation) ‰ Because these pathways are laid down first, they are located in the midline of the CNS and ventral parts of the brain - therefore are most protected ‰ These pathways are not dependent on sensory input for their development

10. PRs and BI ‰ Primitive Reflexes are always firing ‰ PRs fire rostrally to help push the development of the brain ‰ As the brain develops, higher level brain centers fire back down to the brainstem to inhibit the PRs ‰ As these higher-level brain centers fail due to trauma or neurodegeneration, the PRs are recruited. As they re emerge from the brainstem, they are activated to sustain life.

11. Frontal Release Signs ‰ Based on the theory that primitive reflexes become inhibited once frontal lobes become myelinated; when the frontal lobes degenerate, become diseased or are injured, these infantile reflexes then become “released.” ‰ A return of primitive reflex activity is considered to be a sign of disorders that affect the frontal lobes However the affected area is not necessarily confined to the frontal lobes.

12. Primitive Reflexes & Brain Decline ‰ A recent study found that Primitive reflexes were exhibited by 33.1% of aging subjects. Subjects with active PR demonstrated decreased performance on tests evaluating global cognition, executive functions, attention, and language. ‰ The Snout reflex was the most common PR, followed by glabellar tap and palmomental reflex. -Camarda, C. Another recent study found that the palmomental reflex (PMR) could be elicited in 46% of ALS patients. -Taiello A, C

13. Primitive Reflexes & Brain Decline ‰ The Snout reflex: Lightly tapping on the upper lip, just under the nose, causes pouting or pursing of the lips. ‰ Glabellar Tap: A person continues to blink when tapped more than 5 times lightly between the eyebrows. ‰ Palmomental reflex: Stimulation of the thenar eminence can cause an involuntary contraction of the mentalis muscle of the chin.

14. MORO’S REFLEX The reflex is elicited by pulling up on the infant's arms while in a supine position and letting go of the arms causing the sensation of falling The normal Moro reflex starts with the abduction of the upper extremities and extension of the arms. The fingers extend, and there is a slight extension of the neck and spine. After this initial phase, the arms adduct and the hands come to the front of the body before returning to the infant's side.

15. Significance The absence or premature disappearance of the Moro reflex can result from a birth injury, severe asphyxia during the birthing process, intracranial hemorrhage, infection, brain malformation, general muscular weakness of any cause, and cerebral palsy of the spastic type Asymmetrical Moro can be due to a local injury. Damage to a peripheral nerve, cervical cord, or a fracture of the clavicle are common causes to an asymmetric Moro and causes inhibition of the reflex on the affected side Prolonged retention of the Moro reflex can also be a sign of spastic cerebral palsy

16. The Reflex Center Katona 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. Hanabusa 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.

17. The Reflex Center Rönnqvist et al. reported that the average latency of the Moro reflex in 15 term neonates in the quiet awaking state detected with an optoelectronic device was 117.0 ms on the right arm and 129.2 ms on the left. 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 Thus, the center of the Moro reflex seems to be in the lower region of the pons to the medulla.

18. Afferent and Efferent Pathways The head drop, the most common way of eliciting the reflex, stimulates both the vestibular system and the proprioceptive receptors in the neck. Rönnqvist investigated the reflex by tilting the table without extension of the infants’ neck to eliminate the proprioceptive inputs from the cervical vertebrae and neck muscles. The response could be elicited in 225/250 trials (90%), and twenty-one of the 25 negative trials were made while the infants were sleeping or crying. 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

19. The routes of afferent pathways can be multiple, and the efferent pathways of the response seem to originate in the vestibulospinal and/or reticulospinal neurons , because the response can even be obtained in anencephalic newborns devoid of both corticospinal and rubrospinal neurons Thus, t he reflex movement is generated by the subcortical structures without cortical participation , which explains why focal cerebral injury does not cause distinct disturbance of the Moro reflex The primary motor cortex and nonprimary motor areas project a lot of neurons to different motor centers in the brain stem including vestibulospinal and reticulospinal neurons. The brain stem also receives inputs from the basal ganglia and cerebellum. The Moro reflex in infants disappears with age, due to the increased inhibition of these upper brain structures.

20. Palmar/grasp reflex: Emerge: 10 GW ; Integrate: 3 m PN The palmar grasp reflex appears at birth and persists until 5 or 6 months of age replaced by voluntary grasp at 45 months. It requires dual stimulus for eliciting.

21. First by distally moving deep pressure over a specific area of the palmar surface of the hand which elicits a brief muscular contraction (the catching phase), this then develops into a strong holding phase only if traction is made on the tendons of the flexor or adductor muscles, now in contraction, the response being maintained by continued traction. Clinical significance: Spastic form of cerebral palsy and Kernicterus show exceptionally strong grasp reflex whereas it is asymmetrical in cerebral damage and hemiplegia

22. Spinal Reflex Center and Higher Brain Mechanism Because anencephalic infants demonstrate a positive grasp reflex in both the hands and feet, the cerebral hemispheres are apparently not necessary for the reflexes Shahani et al. reported that the latency of the palmar grasp reflex was 40 msec on direct electrical stimulation of the afferent fibers in the median and ulnar nerves at the level of the wrist in an adult patient who showed the palmar grasp reflex following a vascular lesion in the cerebral hemisphere. 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.

23. 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 Adult patients with lesions in the frontal lobes sometimes exhibit a grasp reflex of the hands and feet 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.

24. 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 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.

25. Consequences of Activation Palmar Reflex: Residual effects ‰ Poor pencil grip ‰ Tactile hypersensitivity ‰ Poor thumb and finger opposition ‰ Poor finger dexterity ‰ Difficulty writing, typing, or playing musical instruments

26. However, a weak reflex before six months or persistence of the reflex even after six months implies an underlying abnormality. A weak response presents in peripheral nerve involvement, such as an injury to the roots, plexus, or the spinal cord. Persistence of the reflex beyond six months is usually present in spastic cerebral palsy. It can also reappear in adulthood, indicating a cortical lesion affecting the medial or lateral frontal cortex (e.g., ischemic or hemorrhagic stroke) The injury to the higher center removes the cortical inhibition leading to the release of the primitive reflex

27. Landau reflex The Landau reaction is elicited by supporting the infant horizontally in the air in the prone position. The reaction is present if the infant raises his head and arches his back with the concavity upwards. A subsidiary part of the response is partial extension of the lower limbs at the hip-joints .

28. The reaction may be elicited in normal infants from the age of about 3 months onwards, is present in most infants in the second six months of life, and becomes increasingly difficult to evoke after the age of one year. Absence of the response in infants over the age of 3 months is seen in association with motor weakness, as in cerebral palsy, motor neurone disease and mental retardation. The Landau reaction represents the combined effects of labyrinthine, neck and visual reactions

29. Defining Reflex Patterns Fear Paralysis Reflex Emerge: 5 GW Integrate: 9-12 GW ‰ A withdrawal reflex ‰ The embryo reacts to stress and stimulation by withdrawing and freezing ‰ As the fetus’ tactile awareness develops, withdrawal upon contact gradually lessens Consequences of Activation Fear paralysis reflex: Panic Attacks, Freeze, irregular breathing, severe avoidance

30. Therapeutic Interventions Fear Paralysis Reflex: Tapping - Emotional Freedom Technique, or EFT, a psychological acupressure technique ‰ Light therapy ‰ Meditation ‰ Breathing exercises

31. Snout Reflex Integrate: 12 m PN ‰ Tapping the upper lip lightly near the midline, causes contraction of the muscles of the mouth to resemble a "Pout“ or snout. ‰ One of several reflexes associated with developing facial muscle tone needed for nourishment, articulation and social engagement.

32. Consequences of Activation Snout Reflex: Soft sign of bilateral cerebral damage, associated with pseudobulbar palsy ‰ Affects social engagement ‰ Facial expression ‰ Expressive language

33. Rooting Reaction Emerge: 28GW Integrate: 3 m PN ‰ Needed to search for food ‰ A tactile stimulus to cheek causes infant to turn head and eyes to stimulus ‰ One of several reflexes associated with nourishment and articulation

34. ORAL REFLEXES Rooting reflex: It is present at birth. It begins at 28 weeks IU and becomes well established by 32- 34 weeks IU life. It disappears by 3-4 months of age.

35. A normal response is said to occur when the cheek of a newborn touched or stroked along the side of the mouth causes him to turn the head towards the stimulated side and begins to suck. Clinical significance: Persistence can interfere with sucking and absences is seen in neurologically impaired children

36. Consequences of Activation Rooting Reaction: ‰ Poor articulation ‰ Difficulty swallowing ‰ Difficulty reading out loud

37. Glabellar Tap Reflex Integrate: 4 m PN ‰ Glabellar reflex (also known as the "glabellar tap sign") repetitive tapping on the forehead causes the eyes to blink in response to the first several taps. ‰ Afferent signals travel via the trigeminal nerve, synapsing with efferent signals via the facial nerve that cause the orbicularis oculi muscle to contract (blinking).

38. While suppression of the glabellar reflex may not occur and/or may take longer to occur during childhood development, lack of habituation in adults is categorized as a pathologic sign (often called Myerson’s sign). Myerson’s sign is present in many older individuals. It is associated with many brain conditions, including, but not limited to, dementia and parkinsonism .

39. Consequences of Activation Glabellar Tap Reflex: ‰ Persistent eye closure ‰ Blepharospasm (eyelid twitch) ‰ Common with Parkinson's, Alzheimer’s, frontal lobe infarctions, brain tumors

40. Babkin Palmomental Stimulation of the thenar eminence can cause an involuntary contraction of the mentalis muscle of the chin. This reflex is known as the palmomental or palm-chin reflex. Emerge: 9 GW ; Integrate: 3 m PN

41. NEUROPHYSIOLOGICAL CHARACTERISTICS A stimulus of sufficient strength produces a contraction of the mentalis muscle in all subjects. The common afferent pathway consists of the cutaneous and muscular receptors of the thenar eminence and the median nerve. The common efferent pathway involves the motor nuclei of the facial nerve. Longer latencies may involve the thalamus and motor cortex and shorter latencies may result from brainstem integration of the reflex. Bilateral or contralateral responses were more frequently observed in parkinsonian patients than in younger people. These observations have led to suggestions that cortical inhibition of reflex and decussating brainstem pathways is lost with aging and disease states.

42. Tonic labyrinthine reflex (TLR): It appears at birth and is fixed gradually from 6 weeks to 3 years. TLR stimulus is a change in head position (forward or backward) and response is a change in muscle tone, either flexion or extension. In flexion, the baby's legs are curled up and flexed into the fetal position. Reflex is needed to help babies through the birth canal.

43. Clinical significance: Retained reflex leads to spatial problems, motion sickness, poor posture, muscle tone, and visual perception difficulties. In prone position, the child is in excessive flexion and may not be able to lift or turn the head to clear the air passage. In supine position, the severely involved child is in stiff extension and cannot lift head, bring hands to midline or turn over.

44. Asymmetrical Tonic Neck Reflex (ATNR)

45. Babinski Reflex Emerge: 1 wk PN Integrate: 9 m PN ‰ Important for assisting with the commando crawl, toe differentiation, and balance ‰ A stimulus to the lateral portion of the foot causes toes to flare

46. Babinski ‰ “Pathological reflexes" ‰ The best known (and most important) of the so-called "pathological reflexes" is the Babinski response (upgoing toe; extensor response). ‰ The full expression of this reflex includes extension of the great toe and fanning of the other toes. ‰ This is actually a superficial reflex that is elicited in the same manner as the plantar response (i.e., scratching along the lateral aspect of the sole of the foot and then across the ball of the foot toward the great toe).

47. Babinski ‰ This is a primitive withdrawal type response that is normal for the first few months of life and is suppressed by supraspinal activity sometime before 6 months of age. ‰ Damage to the descending tracts from the brain (either above the foramen magnum or in the spinal cord) promotes a return of this primitive protective reflex, while at the same time abolishing the normal plantar response. ‰ The appearance of this reflex suggests the presence of an upper motor neuron lesion.

48. The Babinski reflex tests the integrity of the corticospinal tract (CST). The CST is a descending fiber tract that originates from the cerebral cortex through the brainstem and spinal cord. Fibers from the CST synapse with the alpha motor neuron in the spinal cord and help direct motor function. The CST is considered the upper motor neuron (UMN) and the alpha motor neu ron is considered the lower motor neuron (LMN). Sixty percent of the CST fibers originate from the primary motor cortex, premotor areas, and supplementary motor areas. The remainder originates from primary sensory areas, the parietal cortex, and the operculum. Damage anywhere along the CST can result in the presence of a Babinski sign.

49. Infants Primitive reflexes are important in the newborn neurological examination. An absent or abnormal sucking reflex is an indirect indicator of neurological maturity in newborn infants. When an abnormal sucking reflex is associated with other signs of CNS involvement, it suggests basal ganglia or brainstem dysfunction. In a 2011 study, morbidity-related factors statistically correlated with the sucking and Babinski reflexes. Moro reflex is weak in preterm infants compared to full-term infants due to their poor muscle tone and resistance to passive movements

50. This response correlates with a delay in motor development in very low birth weight infants. The absence of the Moro reflex suggests CNS dysfunction. Persistence of primitive reflexes past 4 to 6 months or absence before this time when they should have been present is predictive of cerebral palsy The presence of 5 or more abnormal reflexes correlated with the development of cerebral palsy or mental delays

51. Adults Primitive reflexes, also known as frontal release signs, can be normal in the adult population. Multiple frontal release signs observed on neurological examination correlate with frontal lobe brain pathology, including Alzheimer disease, multiple sclerosis, and schizophrenia. Patients with schizophrenia were found to have more frontal release signs than their unaffected siblings and the control group In a 2005 study, researchers detected grasp and Babinski reflex responses in patients with dementia. A present Babinski reflex is important in evaluating a suspected pyramidal tract lesion and is an upper motor neuron damage sign

52. The reappearance of the grasp reflex has been associated with frontal lobe lesions and can be an early sign in corticobasal syndrome, Lewy body dementia, and progressive supranuclear palsy The glabellar tap and palmomental reflexes can be seen as an early sign of Parkinsonian disorders as well The presence of primitive oral reflexes must be distinguished from tardive dyskinesia in patients exposed to neuroleptics. The sucking and rooting reflexes may indicate diffuse cerebral atrophy, while the snout reflex suggests a frontal lobe lesion

53. AFFERENT CENTRE E FFERENT ABNORMALITY CONDITIONS IN WHICH SEEN MORO’S REFLEX Vestibular nuclei lower region of the pons to the medulla vestibulospinal and/or reticulospinal neurons Asymmetric in Local injury spastic cerebral palsy PALMAR GRASP afferent fibers in the median and ulnar nerves supplementary motor area (SMA), premotor cortex, and cingulate motor cortex spastic cerebral palsy, cortical lesion affecting the medial or lateral frontal cortex GLABELLAR TAP REFLEX trigeminal nerve the facial nerve dementia and parkinsonism

54. A FFERENT CENTRE E FFERENT ABNORMALITY CONDITIONS IN WHICH SEEN PALMOMENTAL cutaneous and muscular receptors of the thenar eminence and the median nerve brainstem motor nuclei of the facial nerve stroke, multiple sclerosis, motor neurone disease, and cerebral tumours CORNEOMANDIBULAR ophthalmic division of the trigeminal nerve Corticopontine fibres (supranuclear lesion of V cranial nerve) trigeminal motor neurons acute severe head trauma, cerebrovascular disease, multiple sclerosis, Parkinson’s disease, and amyotrophic lateral sclerosis.