Neurological disorders, especially PN, are common in our Brazilian cohort of IBD patients. They are diverse, multifactorial, and more common in women. Despite the mild phenotype in most cases, attention should be given by the general practitioner and gastroenterologist since they are frequently undiagnosed. Further studies are necessary to confirm these findings in populations with different genetic and nutritional backgrounds.

Spinal cord injury (SCI) leads to profound haemodynamic changes. Constant outflows from the central autonomic pattern generators modulate the activity of the spinal sympathetic neurons. Sudden loss of communication between these centers and the sympathetic neurons in the intermediolateral thoracic and lumbar spinal cord leads to spinal shock. After high SCI, experimental data demonstrated a brief hypertensive peak followed by bradycardia with escape arrhythmias and marked hypotension. Total peripheral resistance and cardiac output decrease, while central venous pressure remains unchanged. The initial hypertensive peak is thought to result from direct sympathetic stimulation during SCI and its presence is anaesthetic agent dependent. Hypotension improves within days in most animal species because of reasons not totally understood, which may include synaptic reorganization or hyper responsiveness of alpha receptors. No convincing data has demonstrated that the deafferented spinal cord can generate significant basal sympathetic activity. However, with the spinal shock resolution, the deafferented spinal cord (in lesions above T6) will generate life-threatening hypertensive bouts with compensatory bradycardia, known as autonomic hyperreflexia (AH) after stimuli such as pain or bladder/colonic distension. AH results from the lack of supraspinal control of the sympathetic neurons and altered neurotransmission (e.g. glutamatergic) within the spinal cord. Despite significant progress in recent years, further research is necessary to fully understand the spectrum of haemodynamic changes after SCI.

The effect of volume expansion of extracellular fluid on gastroduodenal resistance to the flow of isotonic saline was assessed in three groups of rats using intravenous infusions of isotonic, isotonic-isoncotic, and isotonicisoncotic-isohaemic solutions. The gastroduodenal segment of 29 male Wistar rats was barostatically perfused at a constant pressure gradient of 4 cm H20 and changes in flow (ml/ minute) were taken as a reflection of changes in gastroduodenal resistance. Isotonic expansion led to a 33% drop in gastroduodenal flow compared with the normovolaemic period in the same animals (p<001). Extracellular fluid expansion with isotonic-isoncotic and isotonic-isoncotic-isohaemic solutions was associated with reductions in gastroduodenal flow of 29% (p<0.05) and 31% (p<0.01) respectively. The increase in gastroduodenal resistance is due to hypervolaemia per se and not to haemodilution, decreases in plasma oncotic pressure, or electrolyte imbalance. The effect of hypervolaemia on gastroduodenal resistance, which was reversed by smalli haemorrhages (0.5-1.0 ml per 100 g body weight), may In a recent report we showed that acute changes in the extracellular fluid volume were followed by changes in the flow of isotonic saline through the antroduodenal segment of dogs. Acute extracellular fluid volume expansion by intravenous infusion of isotonic saline significantly decreased antroduodenal flow. Conversely, retraction (by haemorrhage) greatly increased it. Since the antroduodenal segment was perfused at a constant pressure during the experiment, the changes in flow were assumed to reflect changes in the resistance(s) of this part of the gastrointestinal tract, possibly changes in tonus or phasic motor activity, or both. ' The gastrointestinal tract seems to react to extracellular fluid volume imbalance by adjusting its intestinal absorption/secretion ratio and its motor function. Materials and methods Twenty nine male Wistar rats (190-310 g) were kept for 24 hours without food but with free access to water. The animals were anaesthetised with an intraperitoneal injection of urethane solution (1 2 g per kg) and then underwent tracheostomy. The external jugular or femoral vein and the carotid or femoral artery were cannulated with polyethylene tubing (PE 50). The veins were used for infusion of expanding solutions and drugs, while the arteries were used for bleeding and for blood pressure measurements. Blood pressure (in mmHg) was measured continuously. In most experiments an Hg manometer was used but in group IV we utilised a Statham pressure transducer connected to a polygraph (Narco-Bio-Systems, Houston, Tx, USA). All animals received an intravenous injection of heparin (500 U in 0 1 ml NaCl, 155 mM) to prevent cannula obstruction.The abdomen was opened by midline incision. The small intestine was exposed and sectioned 3 cm distal to the pylorus. The distal end was ligated and the proximal one was cannulated so that the tip of the cannula was 2 cm distal to the pylorus. A gastric probe was introduced...

-The distinction of non-epileptic from epileptic events is difficult even for experienced neurologists. We retrospectively evaluated 59 dialeptic events from 27 patients admitted for video EEG monitoring to check whether heart rate (HR) analysis could help in differentiating dialeptic complex partial temporal lobe seizures (TLS) from dialeptic simple partial TLS, and non-epileptic dialeptic events. Baseline HR was increased in the simple partial TLS in comparison to complex partial TLS and non-epileptic groups (p<0.05). HR increase accompanied each individual dialeptic complex partial TLS (100% of the events, p<0.05) bur HR returned to baseline in the post-ictal phase. Ictal HR was not altered in the non-epileptic or simple partial TLS groups. Our findings suggest that ictal centrally mediated tachycardia is characteristic of dialeptic TLS (both tachycardia and bradycardia have been reported during TLS). This finding may be used as a criterion to distinguish dialeptic complex partial TLS from simple partial and non-epileptic dialeptic events.KEy WORdS: heart rate, dialeptic seizures, temporal lobe epilepsy, epileptic auras. a análise da freqüência cardíaca diferencia crises dialépticas parciais complexas de auras e crises não epilépticas RESUMO -A distinção entre eventos não epilépticos de epilépticos é difícil mesmo para neurologistas experientes. Analisamos 59 eventos dialéticos de 27 pacientes internados para monitorização por video-EEG para checar se a análise da frequência cardíaca (FC) poderia auxiliar na diferenciação de crises dialépticas parciais complexas de crises dialépticas parciais simples e eventos dialépticos não epilépticos. A freqüência cardíaca basal estava aumentada nos pacientes com crises parciais simples em comparação com o período basal dos grupos parcial complexa e não epiléptico (p<0,05). Houve aumento da freqüência cardíaca em cada crise dialéptica parcial complexa (100% dos eventos, p<0,05), mas a FC retornou aos níveis basais na fase pós-ictal. A FC ictal não foi alterada nos grupos de crises não epiléticas e nos pacientes com crises parciais simples. Nossos achados sugerem que a taquicardia ictal com mediação central é característica de crises parciais complexas dialépticas (tanto taquicardia quanto bradicardia têm sido relatados durante crises temporais parciais complexas). Tal achado poderá ser utilizado como critério para diferenciar crises dialép-ticas parciais complexas de crises dialépticas parciais simples e eventos dialépticos não epilépticos. PALAVRAS-CHAVE: frequência cardíaca, crises dialépticas, epilepsia do lobo temporal, auras epilépticas.