Congenital indifference to pain (CIP) is a rare condition in which patients have severely impaired pain perception, but are otherwise essentially normal. We identified and collected DNA from individuals from nine families of seven different nationalities in which the affected individuals meet the diagnostic criteria for CIP. Using homozygosity mapping and haplotype sharing methods, we narrowed the CIP locus to chromosome 2q24-q31, a region known to contain a cluster of voltage-gated sodium channel genes. From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7. The mutations completely co-segregated with the disease phenotype, and nine of these SCN9A mutations resulted in truncation and loss-of-function of the Nav1.7 channel. These genetic data further support the evidence that Nav1.7 plays an essential role in mediating pain in humans, and that SCN9A mutations identified in multiple different populations underlie CIP.

Shoulder pain after stroke occurred in 40% of 123 patients surviving, consenting and not too unwell to participate. This included 52 patients of an original cohort of 205 patients presenting with stroke. Eighty percent of patients made a good recovery with standard treatment Patients with sensory and or motor deficits represent at risk sub-groups.

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Different stroke sites produce different patterns of sensory deficit. The progression from painless sensory deficit to CPSP is not purely quantitative.

Neurogenic pain is defined as pain due to dysfunction of the peripheral or central nervous system, in the absence of nociceptor (nerve terminal) stimulation by trauma or disease. Other terms used to describe some (but not all) forms of neurogenic pain include neuropathic pain, deafferentation pain, and central pain; all these terms are subsumed into the wider expression 'neurogenic pain'. The clinical syndromes representing this type of disorder make up at least 25% of the patients attending most pain clinics. This is undoubtedly proportionately greater than its incidence in chronic pain as a whole, and is a measure of its intractability and of the therapeutic dilemma which it presents. However, neurogenic pain syndromes are much commoner than is perhaps generally recognized: when all categories are taken into account, there are probably more than 550,000 cases in the UK population of 56 million at any one time, i.e. a prevalence of about 1%.

Fifty diabetic patients with chronic painful sensorimotor neuropathy were studied prospectively to clarify the natural history of this condition and the roles of small-fibre damage and concomitant peripheral vascular disease (PVD). Initially, 30 patients had no significant PVD (ankle:brachial Doppler ratio > 1.0). Pain was assessed using a visual analogue scale (0-10 cm), and small-fibre function by thermal limen (TL), heat-pain threshold (HPT), and weighted pinprick threshold (PPT). At follow-up, on average 3.6 years later (range 3.0-4.1), 11 patients had died (6 with PVD) and contact had been lost with 6. Pain scores fell in subjects without PVD (n = 24; median (range), from 4.8 (0.5-10.0) to 2.0 (0.0-9.2) cm, p < 0.001) and also in those with PVD (n = 9; from 5.1 (2.0-8.2) to 2.1 (0.0-8.0) cm, p < 0.05). Seven patients (5 without PVD) became painfree; at presentation, these 7 patients had experienced pain for a shorter period of time. Despite this symptomatic improvement, small-fibre function generally deteriorated in both groups, with significant worsening (p < 0.05) of HPT and PPT in patients without PVD, and in HPT and TL in patients with PVD. Neuropathic pain therefore tends to improve with time and can resolve completely. By contrast, small-fibre function continues to deteriorate, indicating that these peripheral measures do not predict the evolution of painful symptoms. The presence or absence of PVD does not appear to affect the natural history of neuropathic pain or its symptomatology.

Stroke is a common disease often requiring rehabilitation, which may be prolonged by shoulder pain. The true incidence of post stroke shoulder pain has not been fully evaluated. In order to establish this, we undertook a prospective study of 123 consecutive patients with a diagnosis of acute stroke during a 6-month period. Patients were assessed by interview, full rheumatological and neurological examination, 14 days post stroke, for a history of shoulder pain according to predetermined criteria. In addition, Barthel Index, HAD score and pain scores were also recorded. Twenty-five percent of patients developed shoulder pain within 2 weeks of their stroke. There was a statistically significant association with ipsilateral sensory impairment (p < 0.005), abnormal rheumatological examination (p < 0.001) and depression score (p < 0.005). We conclude that post stroke shoulder pain is more common than previously realized and in addition to abnormal shoulder joint examination may also be associated with upper limb sensory impairment. Thorough neurological examination is required to detect sensory loss and hence establish patients at risk. This is probably best done by a structured proforma.

LCT is a simple, inexpensive, and noninvasive method of identifying the neuropathic foot at increased risk of ulceration. Patients with high plantar foot temperatures are at increased risk of neuropathic foot ulceration. A normal or low MFT in the neuropathic foot is a marker of PVD, which confers an increased risk of ischemic foot disease.