Table22.2 later)arearrangedina“checkerboard”distribution.Theinternodes,separatedbynodesofRanvier(arrows) alongthemotoraxonsareuniforminthicknessandlength.(B)Acuteaxonalinjury(upper axon) resultsindegenerationofthedistalaxonanditsassociatedmyelinsheath,withatrophyofdenervatedmyofibers.Bycontrast,acutedemyelinatingdisease(lower axon) producesrandomsegmentaldegenerationofindividualmyelininternodes,whilesparingtheaxon.(C)Regenerationofaxonsafterinjury(upper axon) allowsconnectionswithmyofiberstore-form.TheregeneratedaxonismyelinatedbyproliferatingSchwanncells,butthenewinternodesareshorterandthemyelinsheathsarethinnerthantheoriginalones.(NodesRanvieraremarkedbyarrows;comparewithpanelA.)Remissionofdemyelinatingdisease(lower Fig. 22.2 Pathologicchangesinperipheralneuropathies.(A)Regenerationaftersegmentaldemyelination.Teasedfiberpreparationsallowforexaminationofindividualaxonsofperipheralnerves.Anormalaxon(left) withalongthickdarkmyelininternodeflankedbynodesofRanvier(arrows;comparewith
Fig.
22.1A ).Allmyelininternodesalonghisaxonwouldbeexpectedtobeofsimilarlengthandwidth.Therightaxon,bycontrast,showsasegmentsurroundedbyaseriesofthinlymyelinatedinternodesofunevenlengthflankedonbothendsbynormalthickermyelininternodes(arrows marknodesofRanvier;comparewith
Fig.22.1C ).(B–C)Vasculiticneuropathy.In(B),theperineurialconnectivetissuecontainsaninflammatoryinfiltratearoundsmallbloodvesselsthathasobliteratedavessel.In(C),aspecialstainthatcolorsmyelinatedaxonsdarkbluehueshowsthatthenervefascicleintheupperportionofthisfield(asterisk) haslostalmostallofitslargemyelinatedaxons,incontrastwiththeotherfascicleshown.Suchinterfascicularvariationinaxonaldensityisoftenseenin axon) allowsremyelinationtotakeplace,butthenewinterno desalsoareshorterandhavethinnermyelinsheathsthanflankingnormalundamagedinternodes.
http://ebooksmedicine.net neuropathiesresultingfromvascularinjury.
of damage to random internodes is best visualized when examining a series of internodes along individual axons in teased fiber preparations (
Fig. 22.2A
Peripheral neuropathies exhibit several anatomic patterns.
Polyneuropathies usually affect peripheral nerves in a symmetric, length-dependent fashion. Axonal loss is typically more pronounced in the distal segments of the longest nerves. Patients commonly present with loss of sensation and paresthesias that start in the toes and spread upward. By the time the sensory changes reach the level of the knees, the hands are also affected, resulting in a picture described as “stocking-and-glove” distribution. This pattern is often encountered with toxic and metabolic damage.
Mononeuritis multiplex, in which the damage randomly affects individual nerves, resulting (for example) in a right radial nerve palsy and wrist drop and, at a separate point in time, a left foot drop. Mononeuritis multiplex is often caused by vasculitis.
A simple mononeuropathy only involves a single nerve and is most commonly the result of traumatic injury, entrapment (e.g., carpal tunnel syndrome), or certain infections such as Lyme disease.
Many different diseases may be associated with peripheral neuropathy (
Table 22.1 ). We next discuss selected entities that are prototypical for a specific type of polyneuropathy or that are particularly common.
Table 22.1 Peripheral Neuropathies