[Migraine and neurological disorders].
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Biomedical subjects
Publications and source records attributed to L Gjerstad.
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There have been very few reports on rhythmic variation in thyroid hormone concentrations with a periodicity of 4-6 weeks. In an attempt to evaluate whether such a rhythm is a general phenomenon we studied ten healthy male students with weekly blood samples over 12 weeks for T4, T3 and TSH. No rhythmicity could be demonstrated.
Two patients with herpes zoster ophthalmicus (HZO) who experienced a delayed contralateral hemiparesis, the so-called crossed zoster syndrome, are described. Particular emphasis is paid to the cerebral blood flow (CBF) findings studied with the Xenon-133 inhalation technique using single photon emission computed tomography (SPECT). In a 40-year-old female with right-sided hemiparesis, angiography showed multiple segmental narrowings of the intracerebral arteries. Cerebral computer tomography (CT) scans were normal. The CBF studied 11 months after the HZO showed a generalized reduction of flow which, however, was more pronounced in the left hemisphere. On re-examination 8 months later both the mean hemispheric flow and regional CBF (rCBF) had increased to normal values. In a 66-year-old male with dysphasia and right-sided hemiparesis, cerebral CT scans demonstrated two small deep left-sided infarcts. CBF examination showed a generalized reduction of flow in the left hemisphere. The flow was slightly increased on re-examination 12 months later. These findings suggest that the Xenon-133 inhalation method represents a useful way to demonstrate the CBF pattern in this group of patients.
A patient with undiagnosed myotonic dystrophy presented in pregnancy with a history of severe obstetric and neonatal complications in her two previous pregnancies. Problems arising after cesarean section led to the diagnosis of myotonic dystrophy. The features of this condition and its implications for pregnancy are pointed out. Complications of pregnancy and parturition may be the first symptoms of myotonic dystrophy.
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Intra- and extracellular recordings were made in the transverse hippocampal slice in vitro to study the requirements for the triggering of epileptiform discharges of CA1 cells. Spontaneous and induced epileptiform discharges were produced by adding small amounts of sodium benzyl penicillin. Recorded intracellularly, the epileptiform activity consisted of a burst of action potentials superimposed on a depolarizing wave. Extracellular recordings demonstrated a marked synchronization. The epileptiform activity of the CA1 cells appeared without changes in the passive membrane properties or in the spike generating mechanism. Spontaneous epileptiform discharges of the CA2 cells depended upon a synaptic activation from the CA3 region. Stimulation of afferent fibres evoked an early and a late burst response in the CA2 cells. The long latency burst was caused by a re-excitation from the CA3 region. The early burst response seems to be an intrinsic property of the CA1 cells and may be induced by synaptic activation of either apical or basal dendrites. The findings suggest that synaptic depolarization is necessary for the generation of epileptiform discharges of the CA1 cells.
Synaptic transmission was studied in the CA1 region of transverse hippocampal slices in vitro before and after the addition of the epileptogenic agent sodium benzyl penicillin. The presynaptic fibre volley and the field potential associated with the intracellular EPSP, 'field EPSP', were recorded from the layer of the activated synapses. Addition of penicillin did not change either response. The rising phase of the intracellularly recorded EPSP did not change. However, the peak amplitude and, particularly, the duration of the EPSP both increased. The prolongation of the EPSP may be of importance for the triggering of epileptiform bursts.
1. Extra- and intracellular recordings were made from CA1 cells in hippocampal slices in vitro. The effects of ionophoretically applied GABA on somatic and dendritic regions were studied. 2. Ionophoresis of GABA at dendritic sites gave a reciprocal effect by inhibiting the effect of excitatory synapses close to the dendritic application, while facilitating those lying further away. For example, GABA delivered to the mid-radiatum dendritic region reduced the population spike generated by a radiatum volley, while facilitating the population spike evoked by oriens fibre stimulation. Similarly, when single cells were recorded from, mid-apical dendritic delivery of GABA abolished the synaptically driven discharges evoked by fibres terminating at this part of the dendritic tree, but facilitated the responses to input from fibres terminating on the basal dendrites of the same cell. 3. With intracellular recording two effects were observed. Applied near the soma, GABA induced a hyperpolarization associated with an increased membrane conductance. When applied to dendrites, GABA caused a depolarization also associated with an increased membrane conductance. Both types of GABA applications could inhibit cell discharges, although in some cases the depolarizing response could facilitate other excitatory influences or cause cell firing by itself. 4. Both the hyperpolarizing and depolarizing GABA responses persisted after blockade of synaptic transmission by applying a low calcium high magnesium solution, indicating mediation via a direct effect upon the cell membrane. 5. The reversal potential for the hyperpolarizing GABA effect was similar to the equilibrium potential for the i.p.s.p. evoked from alveus or orthodromically, and was 10-12 mV more negative than the resting potential. The size of the depolarizing response was also dependent upon the membrane potential. By extrapolation an estimated equilibrium potential was calculated as about -40 mV. 6. Our results support the idea that the hyperpolarizing basket cell inhibition at the soma is mediated by the release of GABA. This hyperpolarizing response causes a general inhibition of firing. The dendritic effects of GABA, however, seem to represent another type of inhibition, which by shunting synaptic currents makes possible a selective inhibitory influence on afferents synapsing locally while facilitating more remotely placed excitatory synapses. We propose the term discriminative inhibition for this postulated new type of control of pyramidal cell discharges.
1. Intracellular recordings were made from CA1 pyramidal cells in the hippocampal slice in vitro. The responses to orthodromic and antidromic activation and to ionophoretically applied GABA were studied. 2. The epileptogenic agent sodium benzyl penicillin reduced the recurrent i.p.s.p. evoked by subthreshold antidromic stimulation. Reversal potential studies of the i.p.s.p. and resistance measurements showed that this reduction was mainly due to a decrease in i.p.s.p. conductance. 3. Penicillin also reduced the conductance and associated membrane potential changes induced by ejecting GABA near the soma or into the apical dendritic region. 4. The mixed e.p.s.p.-i.p.s.p. evoked by orthodromic stimulation was converted to a pure depolarizing potential as the i.p.s.p. was blocked. Concurrently the probability of discharge to a constant orthodromic stimulus was increased. Similar changes were seen in a low chloride solution. 5. The time course of the reduction of inhibition was similar to that of the enhanced orthodromic response seen after penicillin treatment. 6. We conclude that reduction of postsynaptic inhibition is partly responsible for the increased probability of orthodromic discharge caused by penicillin. The longer latency all-or-nothing burst seen in some cells, however, seems to require an additional mechanism, although reduced inhibition may facilitate the triggering of this burst.
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Carbamazepine (CBZ) could be dissolved in Glycofurol (polyethylene glycol monotetra-hydrofurfuryl ether) with concentrations up to 100 mg/ml, and the solutions were stable for at least 14 days. Ethanol or benzyl alcohol was added without loss in solubility, while water, human serum albumin or Intralipid always led to immediate precipitation. The effect of a CBZ/Glycofurol solution on focal seizure threshold in the visual cortex in cats was investigated using a cerveau isolé preparation. Fourteen experiments were performed using i.v. injections of CBZ with concentrations ranging from 0.2 to 20 mg/kg. In all experiments with doses greater than 1 mg/kg the CBZ/Glycofurol injections exerted a pronounced and immediate effect on the seizure threshold, while Glycofurol alone was ineffective. On average, seizure threshold increased more than 5-fold with doses in the range of 5-20 mg/kg. Investigating the effect of CBZ/Glycofurol on picrotoxin-induced seizure activity in cats, 2 injections of 5 mg/ml of CBZ immediately stopped the seizure activity as evaluated by electrocorticography, while interictal activity remained.
A 28-year-old man with regularly occurring clusters of complex partial seizures was studied over a total of 224 days. His seizure periods lasted 2-4 days and occurred at intervals of 5-6 weeks. Several parameters were studied. The most striking finding was an increase in the serum concentration of thyroxine prior to and during the seizure periods. The concentrations of urine catecholamines and serum cortisol also varied with the seizure periods, but these hormones increased after the seizure periods had begun. To determine if there is a general 4-6-week rhythm in thyroid hormone concentrations, 12 weekly blood samples from 10 healthy male students were analyzed. No rhythmicity was found.
We investigated mechanisms involved in thyroid hormone action on brain excitability. The effect of acute exposure of triiodothyronine (T3) to rat hippocampal slices in vitro was studied. No significant changes could be detected in prevolley, field excitatory postsynaptic potentials (fEPSP) and population spike amplitude, while there was a minor, nonsignificant trend toward shortening of the population spike latency time. T3 had no effect on penicillin-induced epileptiform activity. There was, however, an active accumulation of radioactively labeled T3 in the slices. A rat cervaux-isolé preparation was used to determine focal seizure thresholds in the visual cortex, and no acute (2-4 h) effects were demonstrated. No significant acute effects of T3 on brain excitability in the hippocampus and visual cortex was observed, despite an active accumulation of T3. Thus, the effect of T3 on brain excitability most likely is due to delayed effects.