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Since 1903, when Morax and Marie proposed their theory of centripetal migration of the tetanus toxin, it has been taught that spread to the nervous system occurs via the peripheral nerves, the toxin ascending in the axis cylinders or the perineural sheaths Modern studies, utilizing uorescein-labeled tetanus antitoxin, have disclosed that the toxin is also widely disseminated via blood or lymphatics, probably accounting for the generalized form of the disease However, in local tetanus, the likely mode of spread to the CNS is indeed by retrograde axonal transport Mode of Action of Tetanus Toxin Like botulinum toxin, the tetanus toxin is a zinc-dependent protease It blocks neurotransmitter release by cleaving surface proteins of the synaptic vesicles, thus preventing the normal exocytosis of neurotransmitter.

Fig. 12-9

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You can also use tab characters, spaces, or other characters to improve the layout of the prompt and to convey your message more clearly. The following command produces the dialog box shown in Figure 8-3:

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The toxin interferes with the function of the re ex arc by the blockade of inhibitory transmitters, mainly GABA, at presynaptic sites in the spinal cord and brainstem Elicitation of the jaw jerk, for example, is normally followed by the abrupt suppression of motor neuron activity, manifested in the electromyogram (EMG) as a silent period (see further on) In the patient with tetanus, there is a failure of this inhibitory mechanism, with a resulting increase in activation of the neurons that innervate the masseter muscles (trismus or lockjaw) Of all neuromuscular systems, the masseter innervation seems to be the most sensitive to the toxin Not only do afferent stimuli produce an exaggerated effect, but they also abolish reciprocal innervation; both agonists and antagonists contract, giving rise to the characteristic muscular spasm as discussed on page 40.

Let s test this code in the Text Editor project. Add a button to the form named btnRead with the Text property Read. Create the following Click event procedure for this button:

and they considered them to be related In the variant described by Tandan and colleagues, an autosomal dominant syndrome of Charcot-Marie-Tooth polyneuropathy was combined with ptosis, parkinsonism, and dementia, again without Lewy bodies or senile plaques Other variants have been described by Schmitt and coworkers and by Mata and colleagues Hudson has reviewed 42 sporadic cases in which ALS-parkinsonism-dementia were combined (see References) Under the title Spastic Pseudosclerosis, Jakob, in 1921, described a chronic disease of middle to late adult life, characterized by abnormalities of behavior and intellect; weakness, ataxia, and spasticity of the limbs (chie y the legs); extrapyramidal symptoms such as rigidity, slowness of movement, tremors, athetotic postures, and hesitant, dysarthric speech; and normal spinal uid The pathologic changes were diffuse and consisted mainly of an outfall of neurons in the frontal, temporal, and central motor gyri, corpus striatum, ventromedial thalamus, and bulbar motor nuclei.

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In one of Jakob s cases, there were also prominent changes in the anterior horn cells and corticospinal tracts in the spinal cord like those of ALS The latter nding gave rise to Wilson s concept of the disease as a corticostriatospinal degeneration A degenerative and probably familial disorder that had been described earlier by Creutzfeldt was considered by Spielmeyer to be suf ciently similar to the one of Jakob to warrant the designation Creutzfeldt-Jakob disease As discussed in Chap 33, the disorder described by Creutzfeldt and Jakob has been a source of endless controversy because of its indeterminate character On the one hand, it has been confused with the subacutely evolving myoclonic dementia, or subacute spongiform encephalopathy, which is now known to be an infection due to an unconventional transmissible prion agent.

In addition to its generalized effects on the motor neurons of the spinal cord and brainstem, there is evidence that the toxin acts directly on skeletal muscle at the point where the axon forms the end plate (accounting perhaps for localized tetanus) and also upon the cerebral cortex and the sympathetic nervous system, in the hypothalamus..

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