Isolated insular infarction eliminates contralateral cold, cold pain, and pinprick perception

Abstract

Abstract-Background: Ganglioside epitopes on Campylobacter jejuni are hypothesized as the key to the development and characterization of Guillain-Barré syndrome (GBS), but a comprehensive theory has yet to be established. A C jejuni gene, cst-II, involved in the biosynthesis of ganglioside-like lipo-oligosaccharide, shows a polymorphism (Asn/Thr51) that affects ganglioside epitopes. Objective: To examine the hypothesis that this polymorphism determines autoantibody reactivity, and thereby neurologic presentations in GBS. Methods: C jejuni isolates were collected from 105 GBS (including its variants) and 65 uncomplicated enteritis patients. The authors examined the frequency of cst-II and polymorphism (Asn/Thr51) in connection with the bacterial ganglioside epitopes, autoantibody reactivities against GM1, GD1a, and GQ1b, and patients' neurologic findings. Results: Neuropathic strains more frequently had cst-II, in particular cst-II (Thr51), than did enteritic ones (85% vs 52%; p Ͻ 0.001). Strains with cst-II (Asn51) regularly expressed the GQ1b epitope (83%), whereas those with cst-II (Thr51) had the GM1 (92%) and GD1a (91%) epitopes. The presence of these bacterial epitopes in neuropathy patients corresponded to autoantibody reactivity. Patients infected with C jejuni (Asn51) more often were positive for anti-GQ1b IgG (56% vs 8%; p Ͻ 0.001) and had ophthalmoparesis (64% vs 13%; p Ͻ 0.001) and ataxia (42% vs 11%; p ϭ 0.001). Patients who had C jejuni (Thr51) more frequently were positive for anti-GM1 (88% vs 35%; p Ͻ 0.001) and anti-GD1a IgG (52% vs 24%; p ϭ 0.006) and had limb weakness (98% vs 71%; p Ͻ 0.001). Conclusions:The genetic polymorphism of C jejuni determines autoantibody reactivity as well as the clinical presentation of Guillain-Barré syndrome (GBS), possibly through modification of the host-mimicking molecule. The GBS paradigm is the first to explain the detailed pathogenesis of a postinfectious, autoimmune-mediated, molecular mimicry-triggering disorder.

Neurophysiology of Skin Thermal Sensations

“…In this respect, the posterior insular cortex has been recently identified to also sub serve a fundamental role in pain processing in humans (263). In light of the potential inhibition that cold exerts on pain (see masking mechanisms operated by lamina I cold-sensitive neurons on heat-pinch-cold sensitive neurons; Spinal Integration section), this observation provides support to the previously proposed hypothesis (62) for which the development of central pain (19,296), as often observed after infarction of the insular cortex, could represent a form of thermosensory deficiency resulting from the sudden lack of temperature-induced inhibition of nociceptive circuits at a cortical level (62). This hypothesis is in line with the view that the ascending thermosensory pathway shares not only anatomical, but also functional properties with the pain pathway (65).…”

“…However, recent neuroanatomical work in primate models (58) along with neuroimaging results from human studies (61,62,157), have repeatedly challenged this view (67). Strong evidence has been indeed provided not only for the fact that other cortical areas than the somatosensory one could be involved in thermal processing, but that in fact these areas could play a more specific role in sub-serving temperature (as well as pain) (263) sensations in humans (19,62,237,296). Amongst these areas, the dorsal margin of the posterior insular cortex has been proposed as the specific area for the cortical processing of both the discriminative (157) and affective (62,251) components of thermal sensations in humans.…”

“…For example, in a recent quantitative sensory analysis, warm and cold hypoesthesia was consistently recorded in patients with constrained cortical lesions located in the insular and parietal cortices (296). Interestingly, lesions of the human insular cortex not only induce thermosensory deficits, but also, these are very often accompanied by the development of central pain (19,296). In this respect, the posterior insular cortex has been recently identified to also sub serve a fundamental role in pain processing in humans (263).…”

A rat is not a monkey is not a human: comment on Mogil (Nature Rev. Neurosci. 10, 283–294 (2009))

“…A lesion of the ascending lamina I fibres in the middle of the lateral funiculus, a lesion of the VMpo or a lesion of dorsal posterior insula (dpIns) can cause the complete and permanent loss of pain and temperature sensation in a contralateral region of the body [5][6][7][8] . Conversely, micro stimulation in either the VMpo or the dpIns in awake humans can cause a well localized report of either sensation 9,10 .…”

Acute reversible cerebellar lesions associated with metronidazole therapy

“…Cortical strokes producing pure or predominant sensory symptoms are rare, and clinical-radiologic correlation has not been properly conducted. 2,6,7 Moreover, there is debate regarding the occurrence of central poststroke pain or paresthesia (CPSP), a distressing sequela of sensory strokes, 8 in patients with cortical stroke. 6,9 In this study, we sought to characterize the sensory syndrome in patients with stroke occurring in the cerebral cortex.…”