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Certain mechanisms that are thought to be operative in the death of cerebral neurons exposed to ischemia or to traumatic forces have also been invoked in spinal cord injury These include release of so-called excitotoxins such as glutamate and exposure of neurons to calcium and to agents that produce free radicals The latter mechanism may explain the salutary effect of high doses of.

tical white matter, internal capsule, brainstem, or spinal cord Usually, when hemiplegia is severe and permanent as a consequence of disease, much more than the long, direct corticospinal pathway is involved In the cerebral white matter (corona radiata) and internal capsule, the corticospinal bers are intermingled with corticostriate, corticothalamic, corticorubral, corticopontine, cortico-olivary, and corticoreticular bers It is noteworthy that thalamocortical bers, which are a vital link in an ascending ber system from the basal ganglia and cerebellum, also pass through the internal capsule and cerebral white matter Thus lesions in these parts simultaneously affect both corticospinal and extrapyramidal systems Attribution of a capsular hemiplegia solely to a lesion of the corticospinal or pyramidal pathway is therefore not entirely correct The term upper motor neuron paralysis, which recognizes the involvement of several descending ber systems that in uence and modify the lower motor neuron, is more appropriate.

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1. Necrosis of mainly type 2 bers; loss of myosin; vacuolar changes 2. Type 2 ber atrophy Necrosis, regeneration, vacuolization

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described above) This category comprises a variety of disorders involving single and multiple nerves, notably trigeminal neuralgia and those due to herpes zoster, diabetes, and trauma (including causalgia, discussed further on); a number of polyneuropathies of diverse type; root irritation, eg, from a prolapsed disc; spinal arachnoiditis and spinal cord injuries; the thalamic pain syndrome of Dejerine-Roussy; and rarely parietal lobe infarction such as the ones described by Schmahmann and Leifer As a rule, lesions of the cerebral cortex and white matter are associated not with pain but with hypalgesia The clinical features that characterize central pain have been reviewed by Schott (1995) Particular diseases giving rise to neuropathic pain are considered in their appropriate chapters but the following remarks are of a general nature, applicable to all of the painful states that compose this group.

The sensations that characterize neuropathic pain vary and are often multiple; burning, gnawing, aching, and shooting or lancinating qualities are described There is an almost invariable association with one or more of the symptoms of hyperesthesia, hyperalgesia, allodynia, and hyperpathia (see above) The abnormal sensations coexist in many cases with a sensory de cit and local autonomic dysfunction Furthermore, the pain may persist in the absence of a stimulus and generally responds poorly to treatment, including the administration of opioid medications These pains are classi ed in clinical work by the mechanism that incited them or the anatomic distribution of the pain Peripheral Nerve Pain Painful states that fall into this category are in most cases related to disease of the peripheral nerves, and it is to pain from this source that the term neuropathic is more strictly applicable.

Pain states of peripheral nerve origin far outnumber those due to spinal cord, brainstem, thalamic, and cerebral disease Although the pain is localized to a sensory territory supplied by a nerve plexus or nerve root, it often radiates to adjacent areas Sometimes the onset of pain is immediate on receipt of injury; more often it appears at some point during the evolution or recession of the disorder The disease of the nerve may be obvious, expressed by the usual sensory, motor, re ex, and autonomic changes, or these changes may be undetectable by standard tests In the latter case, the term neuralgia is preferred The postulated mechanisms of peripheral nerve pain are diverse and differ from those of central diseases Some of the current ideas have been mentioned in the earlier section on chronic pain One mechanism is denervation hypersensitivity, rst described by Walter Cannon.

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