Margrethe Ingeman-Nielsen

Incidence of central post-stroke pain.

&NA; Central post‐stroke pain (CPSP) is a neuropathic pain syndrome characterized by constant or intermittent pain in a body part occurring after stroke and associated with sensory abnormalities in the painful body part. This study describes CPSP prospectively during the first year after stroke and characterizes the cerebrovascular lesions and neurological signs associated with the CPSP syndrome. Two hundred and sixty‐seven consecutively admitted patients younger than 81 years were examined in the first week, at 1, 6 and 12 months after stroke. Sensibility to touch (cotton wool), temperature (20°C and 40°C), and pinprick was studied using the contralateral face and extremity as control. A CT scan was done 8 (median) days (range: 1–34 days) after stroke. Two hundred and seven (78%) patients surviving at least 6 months who were able to communicate reliably formed the basis of the study. Abnormal sensory signs were found at least once in 87 (42%) patients. CPSP was found in 16 (8%) patients of whom all but 1 patient also had evoked dysesthesia or allodynia. Further 1 patient had persistent evoked dysesthesia but denied pain. CPSP was not related to sex or age. In patients with single acute cerebral lesions there were no relation between size or location of the lesions and the presence of CPSP. The pain was light in 6 (3%) patients and moderate to severe in 10 (5%) patients. The pain quality was usually lacerating or aching. Fifteen (94%) patients had decreased temperature, touch and pain sensibility and 9 (56%) reported allodynia to cold stimulation and another 9 (56%) patients reported this to touch. Pain onset was within 1 month after stroke in 10 (63%) patients, between 1 and 6 months in 3 (19%) patients and more than 6 months after stroke in 3 (19%) patients.

Sensory abnormalities in consecutive, unselected patients with central post-stroke pain

&NA; This study examined the sensory abnormalities in an unselected, consecutive group of patients with central post‐stroke pain (CPSP) surviving more than 1 year after stroke. The sensory examination included clinical examination and quantitative measures with detection and pain thresholds to heat and cold stimuli, argon laser, bon Frey hair and determination of stimulus‐response function in the 10–45°C range. Sensory examination was in 11 identified CPSP patients (5 female, 6 male; aged 43–80 years) carried out in the painful area using the contralateral homologue area as reference. Pain rating was performed using the McGill Pain Questionnaire and a VAS scale. All patients had ischemic (MRI verified) infarction. Of the 11 patients with supratentorial lesions, 5 had thalamic lesions; in addition, 7 patients had lesions in the brain stem/cerebellum. Median present spontaneous pain intensity on the VAS scale was 3.3 (range: 0–7.7). All patients had pain in the body part with sensory abnormalities, which in 8 patients extended the area with pain. Warm detection threshold was higher in the pain area in all patients, and all except 1 patient had increased cold detection threshold. Cold and heat pain thresholds were raised as well, but to a lesser degree. Sensibility to touch (bon Frey hairs) and pain (argon laser) were changed in only 4 and 3 patients, respectively. A stimulus‐response curve in the 10–45°C range showed different patterns compared to the non‐affected side. A cold allodynia in the 10–45°C range was present in the painful area in 6 (56%) Of the patients. The results support the theory that damage to the spino‐thalamo‐cortical pathway is a necessary condition in CPSP. It is proposed that the spontaneous pain in CPSP is linked to hyperexitability or spontaneous discharges in thalamic or cortical neurons that have lost part of their normal input.

pH-Profile and regional transit times of the normal gut measured by a radiotelemetry device

The pH of the gut lumen was measured in 39 healthy persons using a pH‐sensitive, radiotransmitting capsule. Thirteen persons were studied twice. The location of the capsule was determined by X‐ray. The pH rose from 6.4 in the duodenum to 7.3 in the distal part of the small intestine. In 17 persons the pH dropped by 0.1–0.8 pH units during the last hours of the small intestinal transit. The pH was 5.7 in the caecum, but rose to 6.6 in the rectum. Gastric residence time was 1.1 h, small intestinal transit was 8 h, and colonic transit time was 17.5 h (median values). The results provide a firmer basis for prediction of the level, and the rate of release of active substance from pH‐dependent sustained‐release oral preparations.

Pathoanatomic correlation between poststroke pathological crying and damage to brain areas involved in serotonergic neurotransmission.

Background and Purpose The aim of the study was to correlate the severity of poststroke pathological crying with lesion size and location. Methods Twelve selected stroke patients were ranked in terms of overall clinical severity of the syndrome of pathological crying, and the size and location of the stroke lesion(s) were determined by magnetic resonance imaging. Results The patients with the clinically most severe pathological crying had relatively large bilateral pontine lesions without lesions in the hemispheres. The intermediate group had bilateral central hemispheric lesions, and the clinically least affected patients had mainly unilateral large subcortical lesions. Conclusions Poststroke pathological crying may be attributable to stroke-induced partial destruction of the serotonergic raphe nuclei in the brain stem or their ascending projections to the hemispheres.

Measurement of gastrointestinal pH and regional transit times in normal children

Summary: Gastrointestinal pH and regional intestinal transit times of a capsule were measured in twelve healthy children aged 8–14 years using a radiotransmitting pH-sensitive capsule. The location of the capsule was determined by fluoroscopy. pH in the stomach was 1.5, but rose to 6.4 in the duodenum (mean values). pH gradually rose in the small intestine and reached an alkaline peak value of 7.4 in the distal part. pH dropped to 5.9 in the cecum but rose to 6.5 in the rectum. Median gastric residence time of the capsule was 1.1 h. Small intestinal transit time was 7.5 h, and colonic transit time was 17.2 h. pH profile and intestinal transit times found in the present study are almost identical to values found in studies on healthy adults. It is therefore concluded that the release pattern of pH-dependent sustained-release tablets in children is likely to be equal to that of adults.

Dementia of depression or depression of dementia in stroke

This study describes the correlation between changes in mood symptoms assessed by the Hamilton Depression Rating Scale (HDRS) and intellectual impairment assessed by the Brief Cognitive Rating Scale (BCRS) and Mattis Dementia Rating Scale (MDRS) in 166 unselected 1‐year survivors after stroke, in whom post‐stroke depression (PSD) has previously been described and validated. The course of intellectual impairment associated with PSD was compared with the course of intellectual impairment in non‐PSD patients. In general, improvement in mood symptoms was correlated with an improvement in intellectual function. However, in 53 PSD patients improvement in intellectual performance was absent, despite the fact that the patients reported being significantly less distressed by dementia symptoms. Antidepressive medication did not lead to any improvement in MDRS score. No evidence was found to support the hypothesis of ‘dementia of depression’. To the contrary, the findings indicate ‘depression of dementia’.

Intellectual Impairment in the First Year following Stroke, Compared to an Age-Matched Population Sample

General intellectual impairment during the first year following stroke in 188 unselected, previously not demented patients aged 60–80 years was assessed with a comprehensive screening test, the Mattis Dementia Rating Scale, and compared to an age-matched population sample. Significant impairment occurred in 32, 26 and 26% of the stroke patients at 1, 6 and 12 months, which correlated to subjective complaints and a dependent life after discharge. Most patients scored stable or improved (84%), while 16% deteriorated significantly. Intellectual impairment correlated to CT lesion size and central atrophy, age and pre-stroke lower functional and social activity, as well as to stroke-induced handicap including aphasia, neglect, and increased mood symptoms. Thus, stroke-induced brain damage influences general intellectual function but may not be the sole reason for intellectual impairment.

Post-stroke pathological crying: frequency and correlation to depression.

While pathological crying has classically been described as a disturbance of the motor concomitants of emotional affect that is unrelated to mood, recent studies indicate that there may in fact be a correlation. We therefore undertook a study of post‐stroke pathological crying in relation to mood score/depression and lesion site in an unselected stroke population the first year following stroke. The study population comprised 211 patients with first ever stroke (median age 69 years, range 25–80). The patients were included in the study within 7 days of the onset of stroke, and follow‐up examinations were made at 1 month, 6 months and 1 year. Computerized tomography brain scans were obtained on Days 5–10. The frequency of pathological crying was 14% at 1 month, 10% at 6 months and 11% at 1 year. The overall 1 year incidence was 19%. Pathological crying correlated significantly to mood score and post‐stroke depression (p < 0.005), as well as to lesion size (p < 0.05), Barthel Index (p < 0.05), Motricity Index (p < 0.005) and intellectual impairment (p < 0.05), but not to lesion location, sex, age, history of stroke or depression, predisposing disease or social distress before the stroke incident Post‐stroke pathological crying was common and persistent in 11% of patients at 1 year and correlated strongly to mood score and post‐stroke depression. The indication for treatment of pathological crying is therefore further strengthened.

Gastrointestinal pH and transit times in healthy subjects with ileostomy.

Gastrointestinal pH in 11 healthy subjects with ileostomy was determined with a pH‐sensitive, radiotransmitting capsule. Median pH was 7.0 in duodenum, dropped to pH 6.3 in the proximal part, but rose to 7.3 in the distal part of the small intestine. In five subjects the pH of the ileostomy effluents was determined with the pH capsule as well as with a pH meter. Median pH was 7.2 measured with the capsule and 7.4 with the pH meter. The difference between the results obtained with the two methods ranged from 0.1 to 0.3 pH units. The median gastrointestinal transit time of the capsule was 10.5 h (range 6.2–12.8 h). Gastric residence time was 0.6 h (range 0.2–3.8 h), and small intestinal transit time was 10.3 h (range 5.6–11.9 h). Thus the small intestinal transit time in ileostomates is slightly increased compared with values reported from studies on subjects with intact gut. However, no statistically significant correlation was found between the small intestinal transit time and the time elapsed after the creation of the ileostomy. We conclude that colectomy does not alter small intestinal pH but seems to increase the small intestinal transit time of single units.

Effect of Olsalazine and Mesalazine on Intraluminal pH of the Duodenum and Proximal Jejunum in Healthy Humans

BACKGROUND Treatment of inflammatory bowel disease with olsalazine causes diarrhoea in 10% of patients. This is claimed to be caused by a drug effect on mucosal transport in the small intestine, which might be reflected in the intraluminal pH. We aimed to study the effect on jejunal pH of olsalazine (Dipentum) and an alternative preparation, slow-release mesalazine (Pentasa). METHODS Thirteen healthy volunteers, seven male and six female, participated in a randomized, crossover study. Steady-state conditions were obtained after ingestion of 2 g or 6 g mesalazine daily or 2 g olsalazine daily for 1 week. The pH of the duodenum and proximal jejunum was measured by using pH-sensitive, radiotransmitting capsules, the location of which was confirmed by fluoroscopy. RESULTS No effect of either drug on duodenal pH was detected. Mean duodenal pH ranged from 6.18 to 6.22. The mean pH of the pre-medication proximal jejunum was 6.02. Mesalazine had no significant effect, but olsalazine significantly increased the pH of the proximal jejunum (mean pH, 6.47). CONCLUSIONS Our results indicate that the effect of olsalazine on jejunal transport of electrolytes and water, observed in experimental studies, also applies to human subjects in steady-state conditions, and adaptation does not occur within 6 days.