[Clinical anamnestic characteristics in neurological work-related medical rehabilitation : Necessity for a qualitative identification of severe restrictions of work ability]. / Klinisch-anamnestische Charakteristika in der neurologischen MBOR : Notwendigkeit einer qualitativen BBPL-Identifikation.

BACKGROUND: Severe restrictions of work ability (SRWA) as a condition for participation in neurological work-related medical rehabilitation (WMR) have not been adequately described up to now. Similarly, the applicability of the screening instrument SIMBO-C for evaluating SRWA in neurological rehabilitation has not yet been answered conclusively. OBJECTIVE: Determination of clinical and anamnestic characteristics of neurological SRWA and assessment of the applicability of the screening instrument SIMBO-C in neurological WMR. MATERIAL AND METHODS: For the identification of SRWA clinical and anamnestic characteristics of 344 rehabilitants were routinely collected. The clinically and anamnestically determined SRWA was described quantitatively and content-analytically and correlated with SIMBO-C. RESULTS: Of the rehabilitants 66% exhibited SRWA. Apart from the established characteristics of SRWA further person and disease-specific factors were found. The SIMBO-C score was significantly higher in the group with SRWA compared to the group without SRWA (45.6 ± 18.9 vs. 31.5 ± 12.5, p < 0.001); however, 31% of the group with SRWA and 50% of the group without SRWA demonstrated a SIMBO-C score ≤ 36 points and thereby a large overlap. The profile of the clinical and anamnestic characteristics in the group with SRWA was homogeneous, regardless of the SIMBO-C score. CONCLUSION: The characteristics of neurological SRWA are mainly qualitatively shaped and may only partly be identified by SIMBO-C. A combined quantitative and qualitative approach is necessary in neurological WMR.

A cost analysis of the first year after stroke - early triage and inpatient rehabilitation may reduce long term costs.

AIM OF THE STUDY: To analyse the costs of stroke in the first year covered by insurance companies and to correlate them with the clinical outcome data. METHODS: We contacted the insurance companies of 172 consecutive stroke patients of a single institution cohort for a detailed report of the stroke costs. A complete data set over one year was obtained from 131 patients (76%). RESULTS: Severity of stroke was significantly associated with increasing total costs (p = 0.0002). The rehabilitation clinic made up 37% of the total costs followed by nursing home with 21% and acute hospital with 21%. Mean cost of stroke per patient was 31,115 CHF in the first year. Costs per patient for inpatient rehabilitation were similar to those for the nursing home after one year; however, the Barthel-index of patients with inpatient rehabilitation increased by 42 +/- 29 points as compared to patients without inpatient rehabilitation by 23 +/- 26 points (p <0.05), and 86% resp. 81% of patients with inpatient stroke rehabilitation lived independently after 6 and 12 months respectively. CONCLUSIONS: The high level of independence after inpatient stroke rehabilitation underlines the importance of patient selection and/or rehabilitation. Therefore, long-term stroke costs may be significantly reduced by an early and careful triage in the case management after stroke and a case-dependent investment in initial costly appearing inpatient rehabilitation.

[Altered cerebral excitability and spreading depression. Causes for the comorbidity of epilepsy and migraine?]. / Erhöhte zerebrale Erregbarkeit und "spreading depression". Ursachen für eine Komorbidität von Epilepsie und Migräne?

Increased co-occurrence and common clinical aspects of epilepsy and migraine lead to the question of a common pathophysiological model of the diseases. Shared genetic risk factors as an explanation for comorbidity could not be proven. Clinical studies underline the unspecific association of migraine and epilepsy. Comorbidity is based on spreading depression as an expression of altered brain state with neuronal hyperexcitability. In comorbid conditions, therapy with valproate, gabapentin, or topiramate may be effective.

Seizure-associated headache in epilepsy.

PURPOSE: Headache is often ignored as a symptom of epileptic seizures. The purpose of this prospective study was to analyze frequency, classification, and characteristics of seizure-associated headache (SH) according to the criteria of the International Headache Society. METHODS: Over a period of 15 months, 341 patients with epilepsy, consecutively evaluated at our outpatient clinic for SH, completed a standardized questionnaire. RESULTS: Of the 341 epilepsy patients, 115 (34%) experienced SH with a pain intensity of 6.1 +/- 1.6 (SD) on the visual analogue scale and a duration of 12.8 +/- 15.7 (SD) h. Seizures were always accompanied by headache in 69 (60%) of these 115 patients. SH occurred in four (3%) of 115 patients only preictally, in 31 (27%) of 115 patients periictally, and in 80 (70%) of 115 patients only postictally. In the majority of the 115 patients (55.7%), SH could be classified as migraine headache, whereas in 36.5%, as tension-type headache. The type of SH was not correlated with sex, an epilepsy syndrome, or a seizure type. Migraine-like SH was significantly associated with a history of migraine (p < 0.001). In 20 (77%) of the 26 patients experiencing migraine-like SH with a history of migraine, the phenomenology of migraine-like SH and migraine attacks was identical. CONCLUSIONS: SH is a frequent, long-lasting, and severe symptom of epileptic seizures, causing major impairment of daily living. A history of migraine significantly increases the risk for developing migraine-like SH.

Different effects of GABAergic anticonvulsants on 4-aminopyridine-induced spontaneous GABAergic hyperpolarizations of hippocampal pyramidal cells--implication for their potency in migraine therapy.

Clinical studies indicate anti-migrane efficacy of the probably GABAergic anticonvulsants valproate and gabapentin. For the GABAergic anticonvulsants vigabatrin and tiagabine, studies about antimigrane efficacy are missing. The aim of this study was to test the GABAergic potency of these drugs in vitro before further clinical studies. Intracellular recordings were obtained from hippocampal pyramidal cells. Spontaneous GABAergic hyperpolarizations (SGH) elicited by 75 microM 4-aminopyridine were used to test the effect of these drugs on GABA-dependent potentials. Tiagabine (0.1 mM) prolonged the duration of SGH. Furthermore, monophasic SGH turned over into triphasic typical GABAergic membrane potential fluctuations within 20 min. In contrast, valproate, gabapentin, and vigabatrin failed to affect SGH up to 60 min of application. The reason for the fast action of tiagabine on SGH may be caused by a faster increase of synaptic GABA levels compared with other drugs. As migraine therapy benefits from an augmentation of GABA activity, we recommend clinical studies of tiagabine as a fast-acting agent in migraine attacks.

Moclobemide reduces intracellular pH and neuronal activity of CA3 neurones in guinea-pig hippocampal slices-implication for its neuroprotective properties.

Mechanisms underlying the neuroprotective properties of the weak MAO-A inhibitor moclobemide are not understood. Increasing evidence suggests that a moderate increase in intracellular free protons may contribute to neuroprotective properties due to a proton-mediated decrease in neuronal activity. Therefore, we studied effects of 10-700 microM moclobemide (i) on the intracellular pH (pH(i)) of BCECF-AM loaded CA3 neurones as well as (ii) on spontaneous action potentials and epileptiform activity (induced by bicuculline-methiodide, caffeine, or 4-aminopyridine) of CA3 neurones in the stratum pyramidale. Moclobemide-concentrations of > or = 300 microM reversibly reduced the steady-state pH(i) by up to 0. 25 pH-units within 5-20 min. Simultaneously, the frequency of spontaneous action potentials and epileptiform discharges became depressed. Moclobemide also abolished 4-aminopyridine-induced GABA-mediated hyperpolarisations suggesting that the inhibitory and acidifying effects of moclobemide do not result from an amplification of the GABA system. The stronger MAO-A inhibitors clorgyline or pargyline (both 10 microM) mimicked the moclobemide-effects. Investigating effects on pH(i)-regulation we found that 700 microM moclobemide impaired the recovery from intracellular acidification elicited by an ammonium prepulse which demonstrates an impairment of transmembrane acid extrusion. We suggest that the latter effect is responsible for the moderate decrease in the steady-state pH(i) which in turn reduced neuronal activity. This mechanism may substantially contribute to the neuroprotective properties of moclobemide.

Alteration of intracellular pH and activity of CA3-pyramidal cells in guinea pig hippocampal slices by inhibition of transmembrane acid extrusion.

Transmembrane acid extruders, such as electroneutral operating Na(+)/H(+)-exchangers (NHE) and Na(+)-dependent Cl(-)/HCO(3)(-)-exchangers (NCHE) are essential for the maintenance and regulation of cell volume and intracellular pH (pH(i)). Both of them are hypothesised to be closely linked to the control of excitability. To get further information about the relation of neuronal pH(i) and activity of cortical neurones we investigated the effect of NHE- and/or NCHE-inhibition on (i) spontaneous action potentials and epileptiform burst-activity (induced by bicuculline-methiodide, caffeine or 4-aminopyridine) and (ii) on pH(i) of CA3-neurones. NHE-inhibition by amiloride (0.25-0.5 mM) or its more potent derivative dimethylamiloride (50 microM) and NCHE-inhibition by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 0.25-0.5 mM) induced a biphasic alteration of neuronal activity: an initial, up to 30 min lasting, increase in frequency of action potentials and bursts preceded a growing and partially reversible suppression of neuronal activity. In BCECF-loaded neurones the pH(i), however, continuously decreased during either amiloride- or DIDS-treatment and reached its steady-state (DeltapH(i) up to 0.3 pH-units) when the neuronal activity was markedly suppressed. Combined treatment with amiloride (0.5 mM) and DIDS (0.5 mM) or treatment with harmaline alone (0.25-0.5 mM), which also continuously acidified neurones via inhibition of an amiloride-insensitive NHE-subtype, induced a monophasic and partially reversible suppression of neuronal activity. As an initial excitatory period failed to occur during combined NHE/NCHE-inhibition we speculate that its occurrence during amiloride- or DIDS-treatment resulted rather from disturbances in volume- than in pH(i)-regulation. The powerful inhibitory and anticonvulsive properties of NHE- and NCHE-inhibitors, however, very likely based upon intracellular acidification - as derived from our previous findings that a moderate increase in intracellular free protons is sufficient to reduce membrane excitability of CA3-neurones.