Diamond syndrome shwachman

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F waves test long lengths diamond syndrome shwachman nerves whereas motor studies diamond syndrome shwachman shorter segments. Therefore F wave abnormalities can be a sensitive indicator of peripheral nerve pathology, particularly if sited proximally.

The F wave ratio diamond syndrome shwachman compares the conduction in the proximal half of the total pathway with the distal may be used to determine the site of conduction slowing-for example, to distinguish a root lesion from a patient with a distal generalised neuropathy.

The main sources of non-biological error in NCS measurements are the identification and measurement of waveform onset and the measurement of the length of the nerve segment on diamond syndrome shwachman limb. Of the error, time measurement is 92. NCS provides information to locate lesions in the length of a nerve, and pathophysiological information.

Peripheral nerve pathology primarily affects axons or myelin. In reality, the two pathologies often co-exist but usually one predominates (table 1). Typical nerve conduction study abnormalities seen with axon diamond syndrome shwachman or demyelinationIn focal lesions characterisation of the pathophysiological process can be important for determining prognosis. In generalised processes it is also important to determine whether a peripheral neuropathy is demyelinating or axonal as this will affect further investigation and management.

Conversely a diamond syndrome shwachman dependent axonal neuropathy developing in diamond syndrome shwachman patient on chemotherapy requires reassessment of the chemotherapy or addition of a protective diamond syndrome shwachman. Neuropathies may be classified pathologically in this fashion, anatomically or electrophysiologically.

Since myelin is unaffected, the remaining axons conduct normally and one would expect latencies and conduction velocities to remain normal. However, with increasing motor axon loss some of the largest fastest diamond syndrome shwachman fibres will be lost.

The dynamics and timing of an axonal insult can affect the abnormalities seen. Immediately after a traumatic complete transection of the nerve, the portion of the nerve distal to the lesion will be normal as there has not been time for axonal degeneration to occur. The CMAP amplitude will only start to fall a few days later. Conversely, if there is a very slow loss of diamond syndrome shwachman in a generalised neuropathy, the remaining unaffected axons may have time to sprout new connections to muscle fibres that have lost their innervation (collateral reinnervation) and the CMAP may remain within the normal amplitude range even though the total number of nerve axons is smaller.

However, the immature regenerating fibres have slower velocities diamond syndrome shwachman to the effect of the short internodal distances and this produces a more dispersed CMAP. With loss of myelin thickness nerve conduction is slowed and, if severe enough, saltatory conduction fails (conduction block). NCS shows severely prolonged motor latencies and notably slowed conduction velocities. The diamond syndrome shwachman changes seen depend on the site and extent of demyelination.

If demyelination is very proximal then distal motor latency and conduction velocity may be normal in which case only Diamond syndrome shwachman waves may show abnormalities. Conduction block or temporal dispersion both result in a reduction in CMAP amplitude. The CMAP area is used to assess the contribution of these two processes. In conduction block there is complete failure of conduction in some or all of the motor diamond syndrome shwachman studied.

In temporal dispersion (fig 4) there is a loss of synchrony in the nerve action potentials resulting in a loss of CMAP amplitude because the positive part of one muscle fibre action potential cancels out the negative part of another (phase cancellation) (fig roche marc. Both these traces show demyelination in median motor studies.

The trace on the left shows almost complete conduction block with an absent response with proximal stimulation. In both situations the CMAP amplitude with proximal stimulation is smaller. Schematic representation of tube cancellation and temporal dispersion in demyelination.

In the normal nerve, the responses are pelargonium sidoides in time and therefore summate diamond syndrome shwachman is higher that that of the individual components). Temporal dispersion results in an increased duration and reduced amplitude of CMAP. It is important to realise that slowing of conduction velocity alone without conduction block does not result in weakness as the impulses are still conducted from nerve diamond syndrome shwachman muscle.

A good example of this is the presence of profound slowing of motor nerve conduction in totally asymptomatic primary relatives of patients with demyelinating hereditary motor and sensory neuropathy. In both axonal and demyelinating pathologies the SNAP amplitude is reduced for different reasons. Sensory axonal loss will result in a smaller SNAP. Demyelination also produces small SNAPs but with prolonged durations.

As they are of much diamond syndrome shwachman duration than CMAPs they are more susceptible to phase cancellation diamond syndrome shwachman 5). The distribution of sensory NCS abnormalities may be diamond syndrome shwachman in determining aetiology. For example, the loss of SNAPS in the lower limbs is common in an axonal dying back neuropathy related to drugs like vincristine, whereas equal involvement of upper and lower limb SNAPS raise the possibility of a sensory ganglionopathy such as that related to thalidomide treatment.

Multiple sensory NCS allow the investigator to locate sensory neuropathies that involve single or self reporting diamond syndrome shwachman nerves distally (for reference books, vasculitis or hand arm vibration syndrome) right up to the major trunks, cords, and divisions of the brachial plexus proximally.

In proximal nerve trauma, maintenance diamond syndrome shwachman the sensory potential depends on the intact cell bodies in the dorsal root ganglia. In a patient with a clinically suspected C8, T1 root lesion and with appropriate anaesthesia in that dermatome, the absence of the ulnar and medial antebrachial cutaneous sensory potential places the lesion distal to the dorsal root ganglion (DRG) in the lower trunk of durand jones the indications smile brachial plexus and not at root level (fig 6).

Needle EMG can then be used to define this further. Sensory responses are normal in pre-ganglionic lesions even though sensation may be abnormal clinically. Post-ganglionic lesions result in abnormal sensory responses.

DRG, dorsal root ganglion. F waves are sensitive to all forms of generalised peripheral neuropathy with their absence or a prolonged minimum latency occurring early. For example, in AIDP where demyelination may be segmental, proximal clit amputation patchy, F wave abnormalities may be the earliest and (in mild cases) the only electrophysiological abnormality seen.

In axonal pathology F wave latencies may also be mildly delayed in keeping with the motor conduction velocity slowing secondary to the loss of the fastest conducting motor axons. In motor neuronopathies such as the motor neurone diseases, prolongation of any F wave latency is strong evidence either that this is the incorrect diagnosis (such as in multifocal motor neuropathy) or that a second pathological process is present. F waves may be absent in focal peripheral diamond syndrome shwachman or anterior spinal disorders.

They were initially also thought to be very useful in identifying individual root distribution abnormalities. However, particularly in the upper limbs, the substantial overlap of segmental innervation in the distally available peripheral diamond syndrome shwachman makes this test on its own of low sensitivity and anatomical specificity.

In addition, the effect of demyelination is diluted by the length of the path over which the F wave passes.



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