SECTION VII THE NERVOUS SYSTEM Gunshot Wound An 18-yearold high school senior was shot in the left thigh as he left school. On examination in the hospital emergency room,he was found to have weakness of his ankle dorsiflexors,evertors,and invertors,toe flexors,and hamstring muscles. He had sensory loss over the lateral aspect of the leg,the dorsal surface of the foot,and the sole of the foot.The sciatic nerve was exposed surgically and found to be severed.A nerve graft was used to repair the interruption.At a subsequent visit to his physician several weeks later,the weakness was present,and the muscle supplied by the sciatic nerve showed marked atrophy.Electromyography in several of these muscles revealed an absence of motor unit discharges,but frequent fibrillations.Over the next year,there was progressive proximal to distal recovery of some motor function.but there was some residual weakness 1.What caused the weakness in the left lower extremity? 2.What caused the sensory loss? 3.Would there also be autonomic changes in the left leg? 4.Why did the miscles supplied by the sciatic nerve undergo atrophy? 5.Why were there no motor unit potentials several weeks after the injury?hy ere there fibrillations at this time?How can fibrillations be distinguished from motor uit potentials by electromyography? 6.What accounts for the progressive proximal to distal recovery in motor function? 7.Why is recovery incomplete? 8.Would there be sensory recovery as well? 9.Where are the cellular materials made that are needed for the regeneration of motor axons?Sensory axons? 10.How are these materials transferred along the growing axons?
SECTION VII THE NERVOUS SYSTEM Gunshot Wound An 18-year-old high school senior was shot in the left thigh as he left school. On examination in the hospital emergency room, he was found to have weakness of his ankle dorsiflexors, evertors, and invertors, toe flexors, and hamstring muscles. He had sensory loss over the lateral aspect of the leg, the dorsal surface of the foot, and the sole of the foot. The sciatic nerve was exposed surgically and found to be severed. A nerve graft was used to repair the interruption. At a subsequent visit to his physician several weeks later, the weakness was present, and the muscle supplied by the sciatic nerve showed marked atrophy. Electromyography in several of these muscles revealed an absence of motor unit discharges, but frequent fibrillations. Over the next year, there was progressive proximal to distal recovery of some motor function, but there was some residual weakness. l. What caused the weakness in the left lower extremity? 2. What caused the sensory loss? 3. Would there also be autonomic changes in the left leg? 4. Why did the muscles supplied by the sciatic nerve undergo atrophy? 5. Why were there no motor unit potentials several weeks after the injury? Why were there fibrillations at this time? How can fibrillations be distinguished from motor unit potentials by electromyography? 6. What accounts for the progressive proximal to distal recovery in motor function? 7. Why is recovery incomplete? 8. Would there be sensory recovery as well? 9. Where are the cellular materials made that are needed for the regeneration of motor axons? Sensory axons? 10. How are these materials transferred along the growing axons?
ANSVER 1.The weakness of the muascles in the distribution of the sciatic nerve was caused by the interruption of this nerve.The pattern of motor loss (weakness of the hamstring museles,as well as of more distal muscles)indicates a proximal location of the interruption.A proxinal location is consistent with the location of the gunshot wound in the thigh.The transection of the sciatic nerve interrupted sciatic nerve notor axons that originated from motoneurons in the ventral horn of the lumbosacral spinal cord.Therefore,motor commands could no longer reach the ruseles supplied by the sciatic nerve.and hence the muscles could not longer be activated. 2.The semsory loss was caused by interruption of sensory axons in the sciatic nerve.The cutaneous sensory loss was in the distribution of the sciatic nerve. Sensory function in muscles and joints would also be lost.The cell bodies of the sensory neuroms of the sciatic nerve are in dorsal root ganglia of the lunbosacral enlargement. 3.Autononic function in the distal part of the left leg would also be lost because the sciatic nerve contains sympathetic postganglionic axons,as well as somatic motor and sensory axons. 4.Skeletal ruscle fibers depend on innervation for their maintemance.Motor axons nay release a trophic factor that provides signals to the nuscle.Denervation deprives the mascle cells of this trophic factor,and it leads to their atrophy and eventual disappearance if the muscle is not reinnervated.Muscle that is not used will also atrophy to some extent ('disuse atrophy").and this type of atrophy is not nearly as profound as denervation atrophy. 5.After complete denervation of a skeletal muscle,motor unit potentials can no longer be observed because these potentials depend on the synchronous activation of a collection of muscle fihers by an individual motor aron.The motor unit,which consists of a motoneuron and all of the muscle fibers that it innervates,is disrupted
ANSWER 1. The weakness of the muscles in the distribution of the sciatic nerve was caused by the interruption of this nerve. The pattern of motor loss (weakness of the hamstring muscles, as well as of more distal muscles) indicates a proximal location of the interruption. A proximal location is consistent with the location of the gunshot wound in the thigh. The transection of the sciatic nerve interrupted sciatic nerve motor axons that originated from motoneurons in the ventral horn of the lumbosacral spinal cord. Therefore, motor commands could no longer reach the muscles supplied by the sciatic nerve, and hence the muscles could not longer be activated. 2. The sensory loss was caused by interruption of sensory axons in the sciatic nerve. The cutaneous sensory loss was in the distribution of the sciatic nerve. Sensory function in muscles and joints would also be lost. The cell bodies of the sensory neurons of the sciatic nerve are in dorsal root ganglia of the lumbosacral enlargement. 3. Autonomic function in the distal part of the left leg would also be lost because the sciatic nerve contains sympathetic postganglionic axons, as well as somatic motor and sensory axons. 4. Skeletal muscle fibers depend on innervation for their maintenance. Motor axons may release a trophic factor that provides signals to the muscle. Denervation deprives the muscle cells of this trophic factor, and it leads to their atrophy and eventual disappearance if the muscle is not reinnervated. Muscle that is not used will also atrophy to some extent ("disuse atrophy"), and this type of atrophy is not nearly as profound as denervation atrophy. 5. After complete denervation of a skeletal muscle, motor unit potentials can no longer be observed because these potentials depend on the synchronous activation of a collection of muscle fibers by an individual motor axon. The motor unit, which consists of a motoneuron and all of the muscle fibers that it innervates, is disrupted
when the axons that connect the motoneuron cell body with the muscle fibers are severed.Fibrillations are spontaneous contractions of denervated individual muscle fihers.They are recognized in electroayography by their narrow and relatively small action potentials.Furthernore.they do not respond to atteapts at voluntary contractions.Motor unit potentials are broader and larger because they represent the compound action potentials of many ruscle fibers.Sone asynchrony in the action potentials of different muscle fibers also occurs. 6.After a motor axon is severed,several events occur.There are retrograde changes in the notoneuronal cell body (chromatolysis).and the axon distal to the lesion degenerates (Vallerian degeneration).Sprouts energe from the distal end of the axon.and if these reach the distal part of the nerve,one of the sprouts vill grow along a row of Schwann cells (band of Bungner).If this axom reaches its previous target muscle,it can reinmervate the muscle and restore its function:the rate of regeneration is about 1 m/day.Naturally,the first muscles to regain function are those nearest the level of the injury.More distal muscles will recover at later tines,provided that regenerating motor axoms reach thea before atrophy is complete. 7.Recovery is incomplete because not all axons will reach their original target destinations.Some sprouts will grow in the wrong direction,others may form a neurona (a tangled web of avonal sprouts.including sensory axons that my produce pain),and still others may follow the wrong row of Schwann cells and innervate the wrong muscle or even other structures.Only reinnervation of the original target will restore normal funetion. 8.Sensory axons regenerate in much the same way as motor axons,and so sensory funct ion may recover as well as motor funct ion.However,in some individuals nerve injury results in a chronic neuropathic pain syndrome. 9.Membrane components and cytoskeletal proteins needed for the regeneration of an axon are manufactured in the cell bodies of motor and sensory neurons. 10.Materials used for regrowth of axons are tramsported froa the cell body along the axon by slow anterograde axonal transport.The rate of this tramsport is about I mn/day,which accounts for the rate of regeneration of the axoms
when the axons that connect the motoneuron cell body with the muscle fibers are severed. Fibrillations are spontaneous contractions of denervated individual muscle fibers. They are recognized in electromyography by their narrow and relatively small action potentials. Furthermore, they do not respond to attempts at voluntary contractions. Motor unit potentials are broader and larger because they represent the compound action potentials of many muscle fibers. Some asynchrony in the action potentials of different muscle fibers also occurs. 6. After a motor axon is severed, several events occur. There are retrograde changes in the motoneuronal cell body (chromatolysis), and the axon distal to the lesion degenerates (Wallerian degeneration). Sprouts emerge from the distal end of the axon, and if these reach the distal part of the nerve, one of the sprouts will grow along a row of Schwann cells (band of Bungner). If this axon reaches its previous target muscle, it can reinnervate the muscle and restore its function; the rate of regeneration is about 1 mm/day. Naturally, the first muscles to regain function are those nearest the level of the injury. More distal muscles will recover at later times, provided that regenerating motor axons reach them before atrophy is complete. 7. Recovery is incomplete because not all axons will reach their original target destinations. Some sprouts will grow in the wrong direction, others may form a neuroma (a tangled web of axonal sprouts, including sensory axons that may produce pain), and still others may follow the wrong row of Schwann cells and innervate the wrong muscle or even other structures. Only reinnervation of the original target will restore normal function. 8. Sensory axons regenerate in much the same way as motor axons, and so sensory function may recover as well as motor function. However, in some individuals nerve injury results in a chronic neuropathic pain syndrome. 9. Membrane components and cytoskeletal proteins needed for the regeneration of an axon are manufactured in the cell bodies of motor and sensory neurons. 10. Materials used for regrowth of axons are transported from the cell body along the axon by slow anterograde axonal transport. The rate of this transport is about 1 mm/day, which accounts for the rate of regeneration of the axons
