Neurophysiology Lecture 5 PDF

Neurophysiology Lecture 5 Prof.dr.heba shawky  Spinal Cord Transection Causes: a. Road accidents that result in fracture of the vertebrae b. Primary tumors or metastasis from malignant tumors Complete Transection (T.S.) of the spinal cord The extent of lesion determines...

Neurophysiology Lecture 5 Prof.dr.heba shawky  Spinal Cord Transection Causes: a. Road accidents that result in fracture of the vertebrae b. Primary tumors or metastasis from malignant tumors Complete Transection (T.S.) of the spinal cord The extent of lesion determines the clinical manifestations. a)Transection at the upper cervical level, results in immediate death due to paralysis of all respiratory muscles. b)Transection at lower cervical level, results in quadriplegia, however, diaphragmatic respiration is still present. c)Transection lower down in the thoracic region, allows normal respiration, but the patient ends up with paralysis of both lower limbs i.e. paraplegia Compete T.S. of spinal cord lead permanent loss all sensations and voluntary movements below the level of the lesion due to section of all sensory and motor tracts. However Spinal Reflexes pass into the following stages: a. Stage of spinal shock It occurs immediately after the transection of the spinal cord. Cause: It is due to the sudden withdrawal of facilitatory supraspinal impulses of the descending pathways i.e. corticospinal, reticulospinal and vestibulospinal tracts. During this period the resting membrane potential of the spinal motor neurons is 2-6 mv greater than normal (hyperpololarized) (RMP became -72 to -76 mv). Duration: variable depending on the degree of encephalization i.e. dominance of cerebral cortex on spinal cord centers. The higher the development of the brain the longer is the duration of spinal shock (2-6 weeks in human).  Manifestations: below the level of the lesion: Loss of all reflexes (superficial, deep and visceral): a. Loss of deep reflexes → absent tendon jerks b. Loss of muscle tone → flaccid muscles and decrease of the efficiency of the muscle pump. Thus, venous return is reduced → cold and blue limbs c. Loss of visceral reflexes (micturition, defecation and erection) d. "Retention with overflow": the tone in the internal urethral (or anal) sphincter returns very rapidly while the urinary bladder and rectal walls are still paralyzed. Thus, urine is retained and accumulates until the pressure in the bladder overcomes the resistance offered by the sphincter, so, dribbling of urine occurs. Loss of vasomotor tone: a. Cause: interruption of connecting fibers between the vasoconistrictor centers and the lateral horn cells of the spinal cord( origin of preganglionic sympathetic). b. The loss of vasoconstrictor tone causes an immediate fall in blood pressure. c. The higher the level of the section, the lower the blood pressure. Bed sores: a. Cause: the body weight hinders the circulation of blood to the skin. The skin "sloughs off", forming ulcers that heal with difficulty "decubitus ulcers". b. Site: particularly over bony prominences i.e. back, heel and gluteal region. This occurs, if the patient mobilization and cleaning of these areas is neglected b. Stage of recovery of reflexes: After the stage of spinal shock ends, some reflex activity is recovered and excitability of the cord centers returns. Cause of recovery of reflexes may be due to: Development of denervation hypersensitivity to the chemical transmitter released by the remaining spinal excitatory endings. Sprouting of collaterals from existing neurons, with the formation of additional excitatory endings on inter neurons and motor neurons Recovery is gradual and includes the following features: Early Recovery: 1. Gradual rise of arterial blood pressure towards normal, due to regaining of activity in the lateral horn cells of the spinal cord, which form the spinal vasomotor centre. However, as vasomotor control from the medulla is absent, the patient develops a sudden fall in blood-pressure on being made to sit up or stand. 2. Return of spinal reflexes a. Flexor reflexes return earlier than extensor ones. Return of flexor tone (stretch reflex) → the lower limbs take a position of slight flexion "paraplegia in flexion". b. The planter reflex shows a positive Babinski sign. c. Deep reflexes e.g. knee jerk, also recover d. Return of spinal reflexes and tone in arterioles and venules improve the circulation through the limbs. 3. Return of visceral reflexes: This is evidenced by the return of automatic function of both bladder and rectum (automatic evacuation), but voluntary control over micturition and sensation of bladder fullness are permanently lost. 4. Mass reflex: It reflects the high excitability of the spinal cord neurons. A minor painful stimulus to the skin of the lower limbs will cause: - Flexion withdrawal of the limb. - Evacuation of the bladder and rectum. - Sweating of the skin. - Rise of blood pressure. Intented mass reflex can be used to give paraplegic patients a degree of bladder and bowel. They can be trained to initiate urination and defecation by stroking their thighs, thus producing an intentional mass reflex. 5. Sexual reflexes: Genital manipulation produces erection and even ejaculation. Advanced Stage of Recovery: Patients rehabilitated by proper management enter into a more advanced stage of recovery (mobilization, use of antibiotics, nutrition and fluid balance, have reduced mortality from 80 to 6%) During that stage: 1. The tone in extensor muscles gradually returns and becomes greater than in flexors, so that the lower limbs become extended, a state known as "paraplegia in extension". 2. Positive supporting reflex becomes well developed and the patient can stand without support. C. Stage of failure of reflexes This stage may occur in some patients; infection, malnutrition and other complications of cord transection inhibit spinal reflex activity