OBJECTIVES--To study the clinical and pathophysiological features of central pain due to damage to the CNS. METHODS--156 patients (mostly with ischaemic strokes, some with infarct after subarachnoid haemorrhage and other cerebral conditions; one with bulbar and others with spinal pathology) with central pain have been investigated clinically and varying numbers instrumentally with respect to quantitative somatosensory perception thresholds and autonomic function. RESULTS--Pain onset was immediate in a minority; and from a week or two up to six years in > 60%. For those with supraspinal ischaemic lesions, the median age of onset was 59; dominant and non-dominant sides were equally affected. Two thirds of the patients had allodynia, including a previously undescribed movement allodynia apparently triggered from group I afferents. Most patients exhibited autonomic instability in that their pain was increased by physical and emotional stress and alleviated by relaxation; cutaneous blood flow and sweating may also be affected. Pain occurred within a larger area of differential sensory deficit. The critical deficit seems to be for thermal and pinprick sensations, which were more pronounced in areas of greatest than in areas of least pain; whereas low threshold mechanoceptive functions, if affected, did not vary between areas of greatest and least pain. Skinfold pinch (tissue damage) pain thresholds were only slightly affected in supraspinal cases, but greatly increased in patients with spinal lesions; thermal (heat) pain did not show this dissociation. CONCLUSION--The pathogenetic hypothesis which seems best to fit the findings is that there is up regulation or down regulation of receptors for transmitters, possibly mainly noradrenergic, over time.

https://jnnp.bmj.com/content/jnnp/61/1/62.full.pdf

Central pain: clinical and physiological characteristics.

Amitriptyline is a tricyclic antidepressant agent which also has analgesic properties. Whether its analgesic effects are linked to its mood-altering activity or attributable to a discrete pharmacological action (or a combination of both) is unknown. Clinical trials demonstrate that oral amitriptyline achieves at least a good or moderate response in up to two-thirds of patients with post-herpetic neuralgia and three-quarters of patients with painful diabetic neuropathy, neurogenic pain syndromes that are often unresponsive to narcotic analgesics. Amitriptyline has also demonstrated efficacy in heterogeneous groups of patients with chronic non-malignant pain. Other possible areas of use for amitriptyline are in patients with fibromyalgia or as an adjuvant for uncontrolled cancer pain, although evidence for the latter application is limited. Adverse events resulting from the antimuscarinic activity of amitriptyline (primarily dry mouth and sedation) are commonly reported, even at the low dosages used for the control of pain. Low starting doses and careful dosage titration may help to minimise these effects. Orthostatic hypotension and tachycardia, sometimes associated with tricyclic antidepressant agents, may also pose a problem in the elderly. In summary, amitriptyline has a valuable place in the treatment of chronic pain conditions that affect the elderly provided that the drug is used judiciously to minimise adverse effects. Importantly, amitriptyline remains the best studied of the antidepressant agents in post-herpetic neuralgia and diabetic neuropathy and is an important and effective treatment option in these syndromes.

Amitriptyline. A review of its pharmacological properties and therapeutic use in chronic pain states.

Central pain syndrome is defined as pain associated with a lesion of the central nervous system. It has a low incidence but is frequently intractable and does not have effective treatment. The cause of central pain is speculative; however, the single common sensory abnormality in patients with central pain is interruption of spinothalamocortical nociceptive pathways. It appears that severe central nervous system lesions, with total destruction of ascending sensory systems, do not lead to a central pain syndrome; and that setting of mild, moderate, or severe disruption of the anterolateral ascending system with partial or complete preservation of the dorsal column/medial lemniscus functions is most frequently associated with central pain syndrome. Furthermore, even during remission, dysesthesias and pain could be triggered by additional afferent input to the large fiber/dorsal column/medial lemniscus system and, once established, they may not be abolished byadditional deafferentation. © 1993 John Wiley & Sons, Inc.

Central pain: "new" syndromes and their evaluation.

A multitude of different diseases can result in bilateral thalamic lesions. These include vascular pathologies requiring prompt therapeutic intervention, such as basilar thrombosis or thrombosis of the internal cerebral veins, as well as tumors, infectious or demyelinating diseases, and toxic-metabolic lesions. Therefore, detailed knowledge of the typical radiological findings for the various diseases is essential for determining the correct diagnosis. This review provides a synopsis of the radiological findings for the most important bithalamic lesions and an overview of the literature.

Differential diagnosis of bilateral thalamic lesions

Pain is an exceedingly common sequel of spinal cord injury (SCI): Bonica reported it in 69% of cases and Levi et al in 64% of 353 patients. The majority of patients with syringomyelia suer from central pain, and a number of other pathological conditions (infarct, tumour) aecting the spinal cord are frequently characterised by pain as a leading symptom. The proportion of patients with head (brain) injury followed by chronic pain is unknown, but is certainly signi®cant, especially when headache is taken into account; central pain is classically seen following infarcts in the cerebral part of the `pain pathway'. ± 7 It is, however, both instructive and salutary to note that the majority of ventroposterolateral thalamic and lateral medullary infarcts do not produce central pain.

/pdf/central-pain-following-spinal-and-supraspinal-lesions-2a8y29ryez.pdf

Central pain following spinal and supraspinal lesions

We describe two patients with acquired immunodeficiency syndrome (AIDS) who developed classic thalamic syndrome (TS) due to Toxoplasma abscesses in the thalamic region. Treatment with amitriptyline provided substantial relief in both patients. Postmortem examination in one case revealed a lesion in the internal capsule and thalamic reticular nucleus. These observations indicate that (1) TS can result from an isolated lesion in the internal capsule and reticular nucleus of the thalamus, (2) cerebral abscess can cause classic TS, (3) central pain can be added to the many pain syndromes that afflict AIDS patients, and (4) an analgesic response to amitriptyline is possible in these patients.

Central pain from cerebral abscess: thalamic syndrome in AIDS patients with toxoplasmosis.

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Central pain from cerebral abscess: thalamic syndrome in AIDS patients with toxoplasmosis.