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Biomedical subjects

P Convers

Publications and source records attributed to P Convers.

At least 19 recordsLinked to original sources

An fMRI study of cortical representation of mechanical allodynia in patients with neuropathic pain.

OBJECTIVE: To investigate cerebral activity associated with allodynia in patients with neuropathic pain. METHODS: The brain responses of 27 patients with peripheral (5), spinal (3), brainstem (4), thalamic (5), lenticular (5), or cortical (5) lesions were studied with fMRI as innocuous mechanical stimuli were addressed to either the allodynic territory or the homologous contralateral region. RESULTS: When applied to the normal side, brush and cold rubbing stimuli did not evoke pain and activated a somatosensory "control" network including contralateral primary (SI) and secondary (SII) somatosensory cortices and insular regions. The same stimuli became severely painful when applied to the allodynic side and activated regions in the contralateral hemisphere that mirrored the "control" network, with, however, lesser activation of the SII and insular cortices. Increased activation volumes were found in contralateral SI and primary motor cortex (MI). Whereas ipsilateral responses appeared very small and restricted after control stimuli, they represented the most salient effect of allodynia and were observed mainly in the ipsilateral parietal operculum (SII), SI, and insula. Allodynic stimuli also recruited additional responses in motor/premotor areas (MI, supplementary motor area), in regions involved in spatial attention (posterior parietal cortices), and in regions linking attention and motor control (mid-anterior cingulate cortex). CONCLUSION: On a background of deafferentation in the hemisphere contralateral to stimuli, enhanced or additional responses to innocuous stimuli in the ipsilateral hemisphere may contribute to the shift of perception from innocuous toward painful and ill-defined sensations.

Basal Ganglia↗

Cognitive effects of precentral cortical stimulation for pain control: an ERP study.

Electrical stimulation of the motor cortex (MCS) is a promising and increasingly used neurosurgical technique for the control of refractory neuropathic pain. Although its mechanisms of action remain unknown, recent functional imaging data suggest involvement of the thalamus, brainstem and anterior cingulate/orbitofrontal cortex. Since some of these areas are also implicated in higher cognitive functions, notably attentional processes, we analysed cognitive ERPs and behavioural performance during an "oddball" auditory detection task in patients submitted to this procedure. Eleven consecutive patients undergoing MCS because of neuropathic refractory pain, ranging in age from 25 to 71 years, were included in the study. ERPs were obtained in all cases both during the application ("MCS-on") and within the 10 min that followed discontinuation of the procedure ("MCS-off"). In five patients, ERPs could also be obtained just before the start of MCS. When the patients' sample was taken as a whole, there were no consistent effects of MCS on the ERPs. There was, however, a significant interaction of MCS action with the patients' age, reflecting a significant delay during MCS of the cognitive responses N2 and P3 (N200 and P300) in the group of patients older than 50 years exclusively. This effect was rapidly reversible after MCS discontinuation. No MCS-related changes were observed in the N1 component. At the individual level, the effect of MCS on the endogenous ERPs was highly variable, ranging from a total stability of ERPs (mostly in younger subjects) to latency differences of tens of milliseconds in the older group. These results, together with recent experiments showing P300 alteration during repetitive transcranial stimulation, suggest that motor cortex stimulation may interfere with relatively simple cognitive processes such as those underlying target detection, and that the risk of abnormal cognitive effects related to cortical stimulation may increase with age. Although the procedure appears on the whole remarkably safe, complementary neuropsychological studies in this category of patients are advised, as well as caution to possible adverse cognitive effects when using MCS in the elderly, notably in the presence of pre-existent cerebral lesions.

Adult↗

[First epileptic seizure in the elderly: electroclinical and etiological data in 341 patients].

This study included 341 subjects aged over 60 years, 174 females and 167 males, (mean age 72-years), who experienced their first epileptic seizure and fulfilled all inclusion criteria over an 8-year period. Data were available from the physical examination, EEG, laboratory tests and CT scan or MRI for all patients. The international classification of epileptic seizures was applied, 41 p.cent of the seizures were generalized and 59 p.cent were partial. Status epilepticus occurred in 8 p.cent of the patients. The EEG recording was contributive to diagnosis or helpful for localizing the epileptic focus in 55 p.cent of the patients. Normal brain imaging was observed in 40 p.cent of the patients. The main etiology was cerebrovascular disease (33 p.cent), acute stroke (27 patients), or more often postvascular epilepsy (87 patients). Other etiologies were degenerative cortical dementia in 7 p.cent of the patients, metabolic and toxic disorders in 11 p.cent, and benign or malignant brain tumors in 6.5 p.cent. Thirty-two percent of the seizures were of unknown origin (cryptogenic seizures). No correlation was found between sex, age, and etiology. An antiepileptic drug treatment was initiated in 77 p.cent of the patients who were given either valproate (43 p.cent), carbamazepine (26 p.cent) or barbiturates (7 p.cent). These findings are in agreement with those reported in the reviewed literature.

Aged↗

Parietal and cingulate processes in central pain. A combined positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) study of an unusual case.

Parietal, insular and anterior cingulate cortices are involved in the processing of noxious inputs and genesis of pain sensation. Parietal lesions may generate central pain by mechanisms generally assumed to involve the 'medial' pain system (i.e. medial thalamic nuclei and anterior cingulate cortex (ACC)). We report here PET and fMRI data in a patient who developed central pain and allodynia in her left side after a bifocal infarct involving both the right parietal cortex (SI and SII) and the right ACC (Brodmann areas 24 and 32), thus questioning the schematic representation of cortical pain processing. No rCBF increase was found in any part of the residual cingulate cortices, neither in the basal state (which included spontaneous pain and extended hypoperfusion around the infarct), nor during left allodynic pain. Thus, as previously observed in patients with lateral medullary infarct, neither spontaneous pain nor allodynia reproduce the cingulate activation observed after noxious pain in normal subjects. Conversely, both PET and fMRI data argue in favour of plastic changes in the 'lateral discriminative' pain system. Particularly, allodynia was associated with increased activity anteriorly to the infarct in the right insula/SII cortex. This response is likely to be responsible for the strange and very unpleasant allodynic sensation elicited on the left side by a non-noxious stimulation.

Brain Mapping↗

Electrical stimulation of motor cortex for pain control: a combined PET-scan and electrophysiological study.

Although electrical stimulation of the precentral gyrus (MCS) is emerging as a promising technique for pain control, its mechanisms of action remain obscure, and its application largely empirical. Using positron emission tomography (PET) we studied regional changes in cerebral flood flow (rCBF) in 10 patients undergoing motor cortex stimulation for pain control, seven of whom also underwent somatosensory evoked potentials and nociceptive spinal reflex recordings. The most significant MCS-related increase in rCBF concerned the ventral-lateral thalamus, probably reflecting cortico-thalamic connections from motor areas. CBF increases were also observed in medial thalamus, anterior cingulate/orbitofrontal cortex, anterior insula and upper brainstem; conversely, no significant CBF changes appeared in motor areas beneath the stimulating electrode. Somatosensory evoked potentials from SI remained stable during MCS, and no rCBF changes were observed in somatosensory cortex during the procedure. Our results suggest that descending axons, rather than apical dendrites, are primarily activated by MCS, and highlight the thalamus as the key structure mediating functional MCS effects. A model of MCS action is proposed, whereby activation of thalamic nuclei directly connected with motor and premotor cortices would entail a cascade of synaptic events in pain-related structures receiving afferents from these nuclei, including the medial thalamus, anterior cingulate and upper brainstem. MCS could influence the affective-emotional component of chronic pain by way of cingulate/orbitofrontal activation, and lead to descending inhibition of pain impulses by activation of the brainstem, also suggested by attenuation of spinal flexion reflexes. In contrast, the hypothesis of somatosensory cortex activation by MCS could not be confirmed by our results.

Adult↗

Haemodynamic brain responses to acute pain in humans: sensory and attentional networks.

Turning attention towards or away from a painful heat stimulus is known to modify both the subjective intensity of pain and the cortical evoked potentials to noxious stimuli. Using PET, we investigated in 12 volunteers whether pain-related regional cerebral blood flow (rCBF) changes were also modulated by attention. High (mean 46.6 degrees C) or low (mean 39 degrees C) intensity thermal stimuli were applied to the hand under three attentional conditions: (i) attention directed towards the stimuli, (ii) attention diverted from the stimuli, and (iii) no task. Only the insular/second somatosensory cortices were found to respond whatever the attentional context and might, therefore, subserve the sensory-discriminative dimension of pain (intensity coding). In parallel, other rCBF changes previously described as 'pain-related' appeared to depend essentially on the attentional context. Attention to the thermal stimulus involved a large network which was primarily right-sided, including prefrontal, posterior parietal, anterior cingulate cortices and thalamus. Anterior cingulate activity was not found to pertain to the intensity coding network but rather to the attentional neural activity triggered by pain. The attentional network disclosed in this study could be further subdivided into a non-specific arousal component, involving thalamic and upper brainstem regions, and a selective attention and orientating component including prefrontal, posterior parietal and cingulate cortices. A further effect observed in response to high intensity stimuli was a rCBF decrease within the somatosensory cortex ipsilateral to stimulation, which was considered to reflect contrast enhancing and/or anticipation processes. Attentional processes could possibly explain part of the variability observed in previous PET reports and should therefore be considered in further studies on pain in both normal subjects and patients with chronic pain.

Acoustic Stimulation↗

Carcinoma associated paraneoplastic peripheral neuropathies in patients with and without anti-onconeural antibodies.

OBJECTIVE: When to suspect a paraneoplastic disorder is a puzzling problem that has not recently been studied in a large series of patients referred for peripheral neuropathy. METHODS: From 422 consecutive patients with peripheral neuropathy, 26 were analysed who concomitantly had carcinoma but no tumorous infiltration, drug toxicity, or cachexia. Their clinical, pathological, and electrophysiological data were analysed according to the presence of anti-onconeural antibodies, the latency between presentation and cancer diagnosis, and the incidence of carcinoma in the corresponding types of neuropathy of the population of 422 patients. RESULTS: Seven patients (group I) had anti-onconeural antibodies (six anti-Hu, one anti-CV2) and 19 did not (groups IIA and B). In group I, subacute sensory neuropathy (SSN) was the most frequent but other neuropathies including demyelinating neuropathies were present. Patients in group II A had a short latency (mean 7.88 months), and a rapidly and usually severe neuropathy which corresponded in 11/14 to an established inflammatory disorder including neuropathy with encephalomyelitis, mononeuritis multiplex, and acute or chronic inflammatory demyelinating polyneuropathy (CIDP). Patients in group IIB had a long latency (mean 8.4 years) and a very chronic disorder corresponding in four of five to an axonal non-inflammatory polyneuropathy. In this population, the incidence of carcinoma occurring with a short latency was 47% in sensory neuronopathy, 1.7% in Guillain-Barré syndrome, 10% in mononeuritis multiplex and CIDP, and 4.5% in axonal polyneuropathy. CONCLUSIONS: Paraneoplastic neuropathies associated with carcinoma are heterogeneous disorders. Neuropathies occurring with a long latency with tumours probably resulted from a coincidental association. Neuropathies which occurred within a few years of the tumour evolved rapidly and corresponded mostly to inflammatory disorders. As dysimmune neuropathies are probably paraneoplastic in a limited number of cases, patients with these disorders should probably not be investigated systematically for carcinoma in the absence of anti-onconeural antibodies, except when the neuropathy is associated with encephalomyelitis and probably with vasculitis. Questions remain concerning CIDP.

Aged↗

Paraneoplastic demyelinating neuropathy, subacute sensory neuropathy, and anti-Hu antibodies: clinicopathological study of an autopsy case.

A patient with anti-Hu antibodies, small-cell lung carcinoma, and autopsy-proven subacute sensory neuropathy had early slowing of motor and sensory conduction velocities. In the peripheral nerves, chronic demyelinating and remyelinating lesions with axonal degeneration were associated with an inflammatory reaction consisting of CD8+ T cells and CD68+ macrophages. On immunohistochemical testing, the patient's serum did not react with normal nerve, suggesting that the Hu proteins were not the target of the inflammatory reaction in the nerve.

Aged↗

Allodynia after lateral-medullary (Wallenberg) infarct. A PET study.

We used PET to study regional cerebral blood flow (rCBF) changes in nine patients with unilateral central pain after a lateral medullary infarct (Wallenberg's syndrome). All patients presented, on the abnormal side, a combination of hypaesthesia to noxious and thermal stimuli and allodynia to rubbing of the skin with a cold object (i.e. abnormal pain to innocuous stimulation). The rCBF responses during allodynia were compared with those obtained during stimulation of the normal side using (i) a cold non-noxious stimulus identical to that applied to the painful side, and (ii) an electrical high-frequency stimulus at painful ranges. Statistical analysis disclosed two abnormal patterns of rCBF change during allodynia. First, there is a quantitative change whereby the blood flow response was out of proportion with the actual intensity of the stimulus, i.e. the pattern of activation by innocuous rubbing of the skin was in our patients identical to that previously reported in response to painful stimuli in normal subjects. This pattern concerned primarily the contralateral thalamus in its lateral half and the primary and somatosensory areas, as well as inferior parietal [Brodmann area (BA) 39/40], anterior insular (BA 6) and medial prefrontal (BA 10) cortices. Thalamic over-activity may reflect abnormal transduction and amplification of sensory inputs after spinothalamic deafferentation. This might be responsible for both increased rCBF in multiple cortical targets and the perceived shift of stimulus intensity from innocuous to painful ranges. The second abnormality associated with allodynic sensation was qualitative. It concerned exclusively the contralateral cingulate gyrus, which did not exhibit the usual pain-related rCBF increase reported in normal subjects. This abnormal cingulate response may account for the peculiar response of lateral medullary infarct patients to allodynic pain, which is not simply perceived as an exaggerated pain sensation, but as a new, strange and extremely unpleasant feeling, not previously experienced by the patients.

Adult↗

Chronic inflammatory demyelinating polyneuropathy associated with carcinoma.

The association of chronic inflammatory demyelinating polyneuropathy (CIDP) and carcinoma has rarely been reported and its relevance is debated. Thirty three consecutive patients with probable or definite CIDP (idiopathic or associated with M protein) were investigated. Three patients with definite CIDP had a concomitant carcinoma. One had an IgM paraprotein. Steroids and intravenous immunoglobulins were effective.

Aged↗

Are somatosensory evoked potential recording and magnetic resonance imaging useful for evaluating the risk of neurologic compromise in rheumatoid arthritis patients with atlantoaxial subluxation?

The objective of this study was to determine whether early somatosensory evoked potential recording and/or magnetic resonance imaging are helpful for evaluating and monitoring the risk of neurologic compromise in rheumatoid arthritis patients. Thirty-seven patients with definite rheumatoid arthritis were studied, including 18 with atlantoaxial subluxation. A physical examination, roentgenograms of the cervical spine, early somatosensory evoked potential recording at all four limbs and magnetic resonance imaging of the cervical spine were done in each case. Alterations in somatosensory evoked potentials and magnetic resonance imaging evidence of compression of the medulla oblongata or spinal cord were found in similar proportions of patients with and without atlantoaxial subluxation. These results support the view that physical findings and changes on plain films of the cervical spine are the most reliable data for evaluating and monitoring the risk of neurologic damage in patients with atlantoaxial subluxation. Somatosensory evoked potential studies and magnetic resonance imaging should be reserved for those cases in which physical and roentgenographic data cannot be collected in a satisfactory manner and for patients who are included in study protocols that require accurate evaluation of lesions.

Adolescent↗

Electrical stimulation of precentral cortical area in the treatment of central pain: electrophysiological and PET study.

The clinical, electrophysiological and haemodynamic effects of precentral gyrus stimulation (PGS) as a treatment of refractory post-stroke pain were studied in 2 patients. The first patient had a right hemibody pain secondary to a left parietal infarct sparing the thalamus, while the second patient had left lower limb pain developed after a right mesencephalic infarct. In both cases, spontaneous pain was associated with hyperpathia, allodynia and hypoaesthesia in the painful territory involving both lemniscal and extra-lemniscal sensory modalities in patient 1, extra-lemniscal sensory modality only in patient 2. Both patients were treated with electrical PGS by means of a 4-pole electrode, the central sulcus being per-operatively located using the phase-reversal of the N20 wave of somatosensory evoked potentials. No sensory side effect, abnormal movement or epileptic seizure were observed during PGS. The analgesic effects were somatotopically distributed according to the localization of electrode on motor cortex. A satisfactory long-lasting pain control (60-70% on visual analog scale) as well as attenuation of nociceptive reflexes were obtained during PGS in the first patient. Pain relief was less marked and only transient (2 months) in patient 2, in spite of a similar operative procedure. In this patient, in whom PGS eventually evoked painful dysethesiae, no attenuation of nociceptive RIII reflex could be evidenced during PGS. Cerebral blood flow (CBF) was studied using emission tomography (PET) with O-labeled water. The sites of CBF increase during PGS were the same in both patients, namely the thalamus ipsilateral to PGS, cingulate gyrus, orbito-frontal cortex and brainstem. CBF increase in brainstem structures was greater and lasted longer in patient 1 while patient 2 showed a greater CBF increase in orbito-frontal and cingular regions. Our results suggest that PGS-induced analgesia is somatotopically mediated and does not require the integrity of somatosensory cortex and lemniscal system. PGS analgesic efficacy may be mainly related to increased synaptic activity in the thalamus and brainstem while changes in cingulate gyrus and orbito-frontal cortex may be rather related to attentional and/or emotional processes. The inhibitory control on pain would involve thalamic and/or brainstem relays on descending pathways down to the spinal cord segments, leading to a depression of nociceptive reflexes. Painful dysesthesiae during stimulation have to be distinguished from other innocuous sensory side effects, since they may compromise PGS efficacy.

Aged↗

Adult first generalized seizure: etiology, biological tests, EEG, CT scan, in an ED.

The purpose of this study was to evaluate adult first seizures in an emergency department by analyzing etiologic and epidemiological data and studying the usefulness of biological screening, electroencephalogram (EEG), and cerebral computed tomography (CT) scan. This was a retrospective study of a 3-year period during which 247 patients were admitted to an emergency department for a first generalized seizure. A CT scan had been performed in 247 patients and an EEG in 209. Etiologies were found to be (1) unknown, (2) alcohol abuse, (3) stroke, and (4) tumor. Early recurrence rate was 18.5%. EEG was of low interest in emergency. The rate of cerebral focal lesions on CT scan was significantly lower when both examination results and EEG were normal. The rate of metabolic abnormalities was 4.9%. It was concluded that (1) a short hospitalization is advisable because of recurrences, (2) recurrence rate does not increase significantly in patients with focal cerebral lesion, (3) metabolic screening is necessary, and (4) CT scan will be an outpatient procedure for most patients.

Adolescent↗