Diss. (sammanfattning) Uppsala : Uppsala universitet, 2006. / Härtill 4 uppsatser.

Diss. Uppsala : Univ., 2002.

Diss. (sammanfattning) Umeå : Univ., 2006. / Härtill 5 uppsatser.

No description available.

<p>The purpose of this study was to investigate the difference in amplitude between M-response from m. Abductor pollicis brevis/m. Pronator quadratus and m. Abductor pollicis brevis/m. Abductor digiti minimi on patients with carpal tunnel syndrome, compared with control subjects. We wanted to see if m. Pronator quadratus is a better alternative than m. Abductor digiti minimi as comparison with m. Abductor pollicis brevis on patients with carpal tunnel syndrome.</p><p>Nerve conduction studies were performed on 20 patients with carpal tunnel syndrome and on 31 healthy subjects.</p><p>The test-retest result shows that this method was reproducible. The amplitude difference of m. Abductor pollicis brevis-m. Abductor digiti minimi, for the patients, was 1,5mV lower and the amplitude for m. Abductor pollicis brevis-m. Pronator quadratus was 2mV lower than for healthy subjects. Two of the patients were outside the 2SD for the m. Abductor pollicis brevis-m. Pronator quadratus difference but not on the m. Abductor pollicis brevis-m. Abductor digiti minimi. This may indicate that m. Pronator quadratus was better than m. Abductor digiti minimi in the comparison with the m. Abductor pollicis brevis amplitude.</p>

<p>Skin temperature is detected through signals in unmyelinated C-fibers and thin myelinated Aδ-fibers in the peripheral and central nervous system. Disorders in thin nerve fibres are important and not rare but difficult to diagnose by the most common neurophysiological methods. In this pilot study different methods for quantitative sensory testing, QST, were compared to give some ideas about which method could be the most efficient to use in order to point out injuries of the sensory system in clinical practice. The comparison was made between Békésy (separate warmand cold thresholds) and Marstock test (combined warm and cold thresholds). The study also included the test persons estimations of the difficulty to perform the tests.</p><p>The study showed that there was no practical difference between the tests and that the test persons estimations did not show any indications that the methods differed in rating of difficulty. Our study did not give reason to stop measuring warm and cold detection thresholds separately, which is the international standard and have some theoretical advantages. We also compared detection thresholds for hand and foot, warmth and cold and for both slow and fast temperature changes to enlighten factors that could affect our measuring data.</p>

<p>Neurography is the most objective and reliable measure of the peripheral nerve function, and it is used to diagnose both local and generalized neuropathies. Neurography can measure both motor and sensory nerve functions. The principle for sensory neurgraphy is to stimulate over the nerve and record proximal or distal from the stimulated electrode.</p><p>At the Department of Clinical Neurophysiology, University Hospital Uppsala, a problem has been identified, in that young adult patients tend to show unexpected abnormal neurography values in relation to the expected, indicated by the reference limits, without clinical correlates. This concerns foremost the sensory amplitudes in median and ulnar nerves. The hypothesis is that the requirement of young adults’ amplitudes is too high. A reference material better including more subjects in this age group may solve the problem.</p><p>Sensory nerve conduction studies were performed in 33 subjects, aged 15-30. The nerve functions were tested on median, ulnar and radial nerves. Surface electrodes were used for both recording and stimulation.</p><p>The result shows that the presently used reference material for some nerves indeed has too high requirement for young adults. After increasing the reference material for younger age groups, the new reference limits has been changed and this should cause fewer false positive findings.</p>

Morphological changes, genetic modifications, and cell functional alterations are not always parallel. Therefore, assessment of skeletal muscle function is an integral part of the etiological approach. The general objective of this thesis was to look into the cellular and molecular events occurring in skeletal muscle contraction in healthy and diseased condition, using a single fiber preparation and a single fiber in vitro motility assay, in an attempt to approach the underlying mechanisms from different physiological angles. In a body size related muscle contractility study, scaling of actin filament sliding speed and its temperature sensitivity has been investigated in mammals covering a 5,500-fold difference in body mass. A profound temperature dependence of actin filament sliding speed over myosin head was demonstrated irrespective of MyHC isoform expression and species. However, the expected body size related scaling within orthologus myosin isoforms between species failed to be maintained at any temperature over 5,500-fold range in body mass, with the larger species frequently having faster in vitro motility speeds than the smaller species. This suggest that apart from the MyHC iso-form expression, other factors such as thin filament proteins and myofilament lattice spacing, may contribute to the scaling related regulation of skeletal muscle contractility. A study of a novel R133W β-tropomyosin mutation on regulation of skeletal muscle contraction in the skinned single fiber prepration and single fiber in vitro motility assay suggested that the mutation induced alteration in myosin-actin kinetics causing a reduced number of myosin molecules in the strong actin binding state, resulting in overall muscle weakness in the absence of muscle wasting. A study on a type IIa MyHC isoform missense mutation at the motor protein level demonstrated a significant negative effect on the function of the IIa MyHC isoform while other myosin isoforms had normal function. This provides evidence that the pathogenesis of the MyHC IIa E706K myopathy involves defective function of the mutated myosin as well as alterations in the structural integrity of all muscle irrespective of MyHC isoform expression.

Remembering previously experienced events can happen as a result of an effortful retrieval attempt. At other occasions, a memory can enter our minds without any apparent effort – or, indeed, intention - to retrieve. Although it has long been appreciated that retrieval from episodic memory is intertwined with cognitive control, the neural mechanisms of memory-control interactions remain unclear. In this thesis I have used functional magnetic resonance imaging (fMRI) and scalp-recorded event-related potentials (ERP) to study the neural basis of episodic retrieval at varying levels of cognitive control. The dorsolateral prefrontal cortex (dlPFC) has been suggested to support a cognitive control mechanism (context processing) which is relevant during various situations that demand maintenance of current goals and rules. Although increased dlPFC recruitment with increasing context processing demands has been demonstrated during episodic retrieval, there are relatively few studies directly comparing the engagement of dlPFC during episodic retrieval with that during other task domains. In Study I, context processing demands were amplified in episodic retrieval, auditory attention and emotion regulation tasks. This led to overlapping dlPFC recruitment in the first two domains and a divergent reliance on ventromedial prefrontal cortex in the emotion domain. Thus, when selection between competing representations needs to be carried out in accordance with the currently relevant goals and task rules, the episodic memory system interacts with domain-general cognitive control mechanisms. Studies II and III explored the reactive nature of retrieval-specific control mechanisms: can we flexibly switch between semantic and episodic retrieval based on the information extracted from a retrieval cue? This was studied using a recognition memory task where the relevant information could with equal probability be supplied by the semantic or the episodic memory system. The fMRI results (Study II) showed that the brain activation during the ‘episodic’ but not the ‘semantic’ trials was expressed in the right prefrontal cortex. As the order of trials was unpredictable, the corresponding changes in brain activation might be evoked by differences in early cue-trace interactions. An event-related potential study (Study III) with the same experimental protocol as in Study II showed that neural processing corresponding to the two trial types diverged as early as in the time window 100-140 ms post-cue onset, thus highlighting the importance of early cue-trace matching in the selection of further retrieval processing. Study IV explored incidental episodic retrieval. Although this form of retrieval is a common experience in everyday life and a disturbing symptom in some psychiatric conditions, it is not clear how such spontaneous expressions of memory are initiated and to what extent the prefrontal cortex is engaged. The fMRI results showed, consistent with Study I, that dlPFC is specifically associated with the intention to retrieve, independently of success. Retrieval success engaged similar networks for incidentally as well as intentionally retrieved memories, comprising the hippocampus, precuneus, ventrolateral PFC, and the anterior cingulate cortex. Collectively, the fMRI and ERP results indicated that incidental retrieval was initiated by early (&lt; 200 ms) oldness estimation carried out on the semantic information extracted from the retrieval cues. Taken together, the results of this thesis indicate that episodic retrieval can be initiated via two routes:  a bottom-up input rising early during the cue processing, and a top-down input provided by the cognitive control processes mediated by the prefrontal cortex.

A deeper understanding of both movement control and the effects of nociceptor inputs on our motor systems is critical for proper clinical diagnosis of musculo-skeletal dysfunctions and for development of novel rehabilitation schemes. In the jaw system, masticatory movements are produced by a central pattern generator (CPG) located in the brainstem. Considerable efforts have been made in deciphering this neuronal network. The present thesis contributes towards an increasingly detailed understanding of its essential elements, and presents a hypothesis of how deep somatic pain (i.e. muscle pain) may be evoked and interferes with the masticatory CPG circuitry. In Paper I, the expression of c-Fos-like protein was used as a molecular marker to visualize brainstem neurons that were active during induced fictive mastication in the anesthetized and paralyzed rabbit. Our findings provide a previously lacking detailed record of the neuronal populations that form the masticatory motor pattern. Certain cells were located in brainstem areas previously suggested to be involved in the masticatory CPG. However, it was a new finding that neurons in the dorsal part of the trigeminal main sensory nucleus (NVsnpr-d) may belong to this circuitry. Paper II focused on the discovered neurons in NVsnpr in an in vitro slice preparation from young rats.  Intracellular recordings allowed us to define two cell types based on their response to depolarizing current. Microstimulation applied to the trigeminal motor nucleus, its reticular border, the parvocellular reticular formation and the nucleus reticularis pontis caudalis, elicited postsynaptic potentials in 81% of the neurons tested. Responses obtained were predominately excitatory and sensitive to gluta-matergic antagonists DNQX or/and APV. Some inhibitory and biphasic responses were also evoked. Bicuculline methiodide or strychnine blocked the IPSPs indicating that they were mediated by GABAA or glycinergic receptors. About one third of the stimulations activated both types of neurons antidromically. Neurons in NVsnpr-d seem to gather all the conditions that can theoretically account for a role in masticatory rhythm generation. In Paper III, the masticatory model system was used to investigate the possible role of muscle spindle primary afferents in development of persistent musculoskeletal pain. Following intramuscular acidic (pH 4.0) saline injections of rat masseter muscles, in vitro whole cell recordings were done from jaw closing muscle spindle somata located in the trigeminal mesencephalic nucleus (NVmes). Compared to control neurons, the somata of afferents exposed to acid had more hyperpolarized membrane potentials, more hyperpolarized thresholds for firing, high frequency membrane oscillations and ectopic bursting of action potentials. These changes in membrane properties lasted for up to 35 days. Within the same time frame experi-mental animals showed hypersensitivity to touch on the skin covering the injected muscle. Similar saline injections also resulted in a significant increase of activity dependent c-Fos expression in NVmes neurons compared to controls. Immuno-fluorescence and lectin binding studies indicated that small-caliber muscle afferents containing known nociceptor markers (CGRP, SP, P2X3, TRPV1 and IB4) and expressing glutamate receptors are found close to the annulo-spiral endings of the NVmes afferents. Combined, our new observations support the hypothesis that excessive release of glutamate, within muscle spindles due to ectopically evoked antidromic action potentials, could lead to development of persistent musculoskeletal pain by activation and/ or sensitization of adjacent muscle afferent nociceptors.