What, if anything, is spinal shock?
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Acute Disease↗
Biomedical subjects
J Noth
Publications and source records attributed to J Noth.
Pathophysiology of chorea and bradykinesia in Huntington's disease.
This article reviews the neurophysiological abnormalities described in Huntington's disease. Among the typical features of choreic movements are variable and random patterns of electromyographic (EMG) activity, including cocontraction of agonist and antagonist muscles. Studies of premotor potentials show that choreic movements are not preceded by a Bereitschaftspotential, therefore demonstrating that choreic movement is involuntary. Early cortical median-nerve somatosensory-evoked potentials have reduced amplitudes and the reduction correlates with reduced glucose consumption in the caudate nucleus. Long-latency stretch reflexes evoked in the small hand muscles are depressed. These findings may reflect failed thalamocortical relay of sensory information. In Huntington's disease, the R2 response of the blink reflex has prolonged latencies, diminished amplitudes, and greater habituation than normal. These abnormalities correlate with the severity of chorea in the face. Patients with Huntington's disease perform simple voluntary movements more slowly than normal subjects and with an abnormal triphasic EMG pattern. Bradykinesia is also present during their performance of simultaneous and sequential movements. Eye movements show abnormalities similar to those seen in arm movements. In Huntington's disease, arm movement execution is associated with reduced PET activation of cortical frontal areas. Studies using transcranial magnetic stimulation show that patients with Huntington's disease have normal corticospinal conduction but some patients have a prolonged cortical silent period. Bradykinesia results from degeneration of the basal ganglia output to the supplementary motor areas concerned with the initiation and maintenance of sequential movements. The coexisting hyperkinetic and hypokinetic movement disorders in patients with Huntington's disease probably reflect the involvement of direct and indirect pathways in the basal ganglia-thalamus-cortical motor circuit.
Basal Ganglia↗
GAP-43 (B-50) and C-Jun are up-regulated in axotomized neurons of Clarke's nucleus after spinal cord injury in the adult rat.
The growth-associated protein GAP-43 (B-50) and the transcription factor C-Jun are involved in regeneration of the injured nervous system. In this study, we investigated the possibility of the induction of GAP-43 and C-Jun in axotomized neurons of Clarke's nucleus (CN) in adult rats, of which a large population undergoes degeneration several weeks after a low thoracic lateral funiculotomy of the spinal cord. In situ hybridization and immunohistochemistry revealed a transient up-regulation of GAP-43 mRNA, C-Jun protein, and its activated, phosphorylated form, peaking around 7 days after injury in preferentially large diameter CN-neurons ipsilateral and caudal to the lesion. Our results document that some populations of axotomized central nervous system neurons, similar to axotomized regenerating neurons of the peripheral nervous system, can up-regulate GAP-43 and C-Jun, even if they are destined to degenerate. This might reflect a transient regenerative capacity, which fails over time.
Animals↗
[Spontaneous intracranial hypotension: a rare cause of chronic headache].
Spontaneous intracranial hypotension is a rare cause of chronic postural headache. We report the case of a 58-year-old woman with a 1.5 year history of chronic headache in upright position, nausea and vomiting. Neurological examination was normal. The Gd-enhanced MRI of the brain showed an abnormal meningeal enhancement over the cerebral convexity. The CSF was normal. Opening pressure during lumbar puncture was 6 cm H2O in the lateral recumbent position. No evidence of underlying systemic, infectious or neoplastic diseases could be detected. The headache was alleviated under theophylline therapy. Spontaneous intracranial hypotension should be considered in the differential diagnosis of chronic postural headache. MRI revealing meningeal enhancement and low opening pressure in lumbar puncture are important findings for the diagnosis of spontaneous intracranial hypotension.
Brain↗
Evidence for a non-orthostatic origin of orthostatic tremor.
OBJECTIVES: Orthostatic tremor was first described by Heilman in 1984. It usually occurs in the legs during stance and decreases markedly during sitting or walking. The aim of this study was to determine if orthostatic tremor is invariably associated with the orthostatic and weight bearing conditions in the arms and legs, and to investigate the features of orthostatic tremor under different levels of peripheral loading. METHODS: Multichannel surface EMG recordings were obtained under different conditions (body posture and peripheral loading) from the proximal arm and leg muscles of seven patients fulfilling the clinical and electrophysiological criteria of orthostatic tremor. RESULTS: In weight bearing positions (stance; weight bearing on the hands on all fours), all patients showed 13 Hz-16 Hz tremor activity, predominantly in the active limb. No tremor activity could be found in a supine position with muscles at rest. Isometric contraction of the limbs in the supine position led to synchronous 13 Hz-16 Hz rhythmic activity in five patients. No tremor was seen when the subjects were suspended in a harness with relaxed legs. Isometric contraction of the legs in this position produced tremor in two patients. A stepwise reduction of the body weight by a harness reduced the tremor activity. Additional loading (10 kg-20 kg) during stance led to an increase in tremor amplitude, but tremor frequency remained unchanged. CONCLUSIONS: Orthostatic tremor is invariably present during stance or other weight bearing positions. It is not, however, always associated with orthostasis. In at least some patients it can be classified as an orthostasis independent action tremor. The failure of peripheral loading to modify tremor frequency indicates that orthostatic tremor may have a central, rather than a peripheral, origin.
Aged↗
Three-dimensional transcranial color-coded sonography of cerebral aneurysms.
BACKGROUND AND PURPOSE: The role of 2-dimensional transcranial color-coded sonography (2D-TCCS) as a diagnostic tool in cases of vascular alteration is unquestioned. The skill of the operator, however, may be responsible for some intertrial variability. The clinical value of a new, workstation-based, 3D reconstruction system for TCCS was evaluated in patients with intracranial aneurysms. METHODS: Thirty patients with 30 intracranial aneurysms were investigated (8 men, 22 women; mean+/-SD age 54+/-17 years). The TCCS examinations were performed with a 2-MHz probe using the power mode. The 3D system (3D-Echotech, Germany) consisted of an electromagnet, which induced a low-intensity magnetic field near the head of the patient. A magnetic position sensor was attached to the ultrasound probe and transmitted the spatial orientation of the probe to a workstation, which also received the corresponding 2D-images from the video-port of the duplex machine. The echo contrast enhancer D-galactose (Levovist, Schering, Germany) was used in all patients to improve the signal-to-noise ratio. All patients underwent presurgical digital subtraction angiography (DSA) to demonstrate the aneurysm. RESULTS: Twenty-nine of 30 angiographically proven intracranial aneurysms (97%) were detected by 3D-TCCS. The aneurysmal diameter estimated by DSA ranged from 3 to 16 mm (mean 7. 2+/-3.6 mm). A comparison of the 3 main diameters of each aneurysm revealed a correlation coefficient of 0.95 between DSA and 3D-TCCS. The 3D determination of the aneurysmal size by 2 experienced sonographers correlated with 0.96. CONCLUSIONS: 3D-TCCS is a new, noninvasive method to investigate intracranial aneurysms. The differentiation between artifacts and true changes of the vessel anatomy is much easier in 3D-TCCS than in conventional 2D-TCCS. The new method yields an excellent correlation with the gold standard, DSA. Because the same 3D-TCCS data can be postprocessed by different investigators, it may be possible to improve reproducibility and increase the objectivity of transcranial color-coded duplex sonography.
Angiography, Digital Subtraction↗
Spontaneous orientation of transplanted olfactory glia influences axonal regeneration.
Transplanted olfactory ensheathing cells (OECs) have previously been demonstrated to support axonal growth and myelination in the adult rat CNS. Here, the capacity of donor OECs to control the direction of axonal regeneration has been investigated following transplantation, as elongated columns, into the thalamus of adult rats. The OECs formed a 'glial bridge' which extended from the thalamus to the hippocampus. Transplanted OECs rapidly adopted a spindle-shaped morphology which was orientated along the vertical axis of the transplant. Numerous host axons grew into the transplants and followed the highly orientated OEC cell matrix across the choroid fissure. Thus, the spontaneous elongation and orientation of donor OECs may support highly directional host axonal growth across natural barriers within the CNS.
Animals↗
Expression of interleukin 6 in the rat striatum following stereotaxic injection of quinolinic acid.
Stereotaxic intrastriatal injection of the naturally occurring N-methyl-D-aspartate (NMDA) agonist quinolinic acid (QA) serves as a valuable in vivo model to study excitotoxic cell damage in the central nervous system (CNS). Although morphological changes such as neuronal loss, glial activation and remote reactions following QA injection have been described in some detail, much less is known about the molecular mechanisms mediating the accompanying glial response. Cytokines are known to play a crucial role in almost all kinds of CNS alterations. We now demonstrate that IL-6, a multifunctional glycoprotein which belongs to the family of neurokines, is expressed endogenously in the rat striatum following QA injection. Using Northern blot analysis, a massive but transient upregulation of IL-6 mRNA could be detected. This started 3 h after QA injection, reached a maximum at 6 h and disappeared within 24 h. That activated microglia are the most likely cellular source of the observed corresponding IL-6 protein expression could be concluded by comparing the immunocytochemical pattern of IL-6 expression and microglial activation. Interestingly, astrocytes initially downregulate their expression of glial fibrillary acidic protein (GFAP) in the excitotoxically injured striatum, but show a delayed increase in GFAP immunoreactivity starting in the periphery of the striatum, subsequently expanding to the core. The early transient IL-6 expression may play an important role in initiating the delayed astrocytic response following excitotoxic cell injury.
Animals↗
Spontaneous longitudinally orientated axonal regeneration is associated with the Schwann cell framework within the lesion site following spinal cord compression injury of the rat.
Spontaneous cellular reorganisation at the lesion site has been investigated following massive spinal cord compression injury in adult rats. By 2 days post operation (p.o.), haemorrhagic necrosis, widespread axonal degeneration, and infiltration by polymorphnuclear granulocytes and OX42-positive macrophages were observed in the lesion site. By 7 days p.o., low affinity nerve growth factor receptor-positive Schwann cells, from activated spinal roots, were identified as they migrated far into the lesion. Between 7 and 14 days p.o., the overlapping processes of Schwann cells within the macrophage-filled lesion formed a glial framework which was associated with extensive longitudinally orientated ingrowth by many neurofilament-positive axons. Relatively few of these axons were calcitonin gene-related peptide (CGRP)-, substance P (SP)-, or serotonin (5HT)-positive; however, many were glycinergic or gamma aminobutyric acid (GABA)ergic. At 21 and 28 days p.o. (the longest survival times studied), a reduced but still substantial amount of orientated Schwann cells and axons could be detected at distances of up to 5 mm within the lesion. Glial fibrillary acidic protein (GFAP) immunoreactivity demonstrated the slow formation of astrocytic scarring which only became apparent at the lesion interface between 21 and 28 days p.o. The current data suggest the possibility of developing future therapeutic strategies designed to maintain or even enhance these spontaneous and orientated regenerative events.
Animals↗
[Acetylsalicylic acid in ischemic insult].
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Anticoagulants↗
High-grade stenosis of the internal carotid artery assessed by color and power Doppler imaging.
PURPOSE: Visualization of carotid artery stenosis is important to improve our understanding of the etiology of ischemic stroke. Two sonographic methods are available for visualizing carotid stenosis: power Doppler imaging (PDI) and color Doppler imaging (CDI). The purpose of this study was to compare the advantages and limitations of these methods in the evaluation of internal carotid artery (ICA) stenosis. METHODS: Thirty-two patients with at least 70% extracranial ICA stenosis were included in this prospective study. All subjects were examined with CDI and PDI. Four criteria were used to evaluate diagnostic accuracy and overall efficacy: identifying the target vessel, determining the causal pathology, evaluating blood flow, and the examiner's confidence in the diagnosis. RESULTS: All patients had high-grade stenosis (17 patients had 70% stenosis, 11 had 80%, 2 had 90% and 2 had pseudo-occlusions of the ICA). PDI was significantly (p < 0.05) superior to CDI in identifying the target vessel and highly significantly (p < 0.01) superior to CDI in evaluating blood flow. There were no significant differences between CDI and PDI in determining the causal pathology or in the examiner's confidence in the diagnosis. CONCLUSIONS: This study demonstrates that PDI is a good additional method to CDI and should be used with it to evaluate ICA stenosis.
Adult↗
Agenesis of the internal carotid artery: color Doppler, CT, and MR angiography findings.
Agenesis of the internal carotid artery (ICA) is a rare finding that can lead to the false diagnosis of an ICA occlusion. We present the case of a young woman with agenesis of the left ICA. Diagnosis was made noninvasively by color Doppler imaging (CDI) in combination with high-resolution CT of the base of the skull. Magnetic resonance angiography confirmed the diagnosis. CDI in combination with CT of the base of the skull allows the diagnosis of ICA agenesis without the use of invasive procedures.
Adult↗
Neurophysiological abnormalities in the Westphal variant of Huntington's disease.
The Westphal variant of Huntington's disease (HD) is a distinct clinical entity of HD characterized by a rigid-hypokinetic syndrome and is often associated with a juvenile onset of disease. Definite genetic differences between the subtypes of HD have not been delineated so far. Here we present the results of a battery of neurophysiological tests including somatosensory-evoked potentials, blink reflexes, long-latency reflexes, and measurement of saccadic velocities in a Westphal HD patient. Although quantitative assessment of his motor performance showed a severe hypokinetic syndrome resembling Parkinson's disease, the results of somatosensory-evoked potentials and blink reflexes were indistinguishable from results obtained in hyperkinetic HD patients. Long-latency reflexes, however, which are typically absent in hyper-kinetic HD patients, were retained in this patient. It is concluded that neurophysiology in HD patients is not a mere reflection of the patient's symptomatology but can give insight into the underlying pathophysiological process.
Adult↗
A novel early component of the cell body response in axotomized Clarke's nucleus neurons revealed by monoclonal antibody Py.
The monoclonal antibody Py was initially developed as a tool for the identification of subpopulations of hippocampal neurons. Recently it has also been demonstrated to be a useful marker for other populations of midbrain and spinal cord neurons in which the antigen showed a strong colocalization with cytoskeletal elements. To assess the possible usefulness of Py as a tool for studying lesion-induced cell body changes, densitometric analysis of altered Py-immunoreactivity (Py-IR) has been compared with that of microtubule-associated protein 2 (MAP2) in Clarke's nucleus following axotomy. One week after a unilateral transection of the dorsal spinocerebellar tract at Th9-10, Py-IR in the Clarke's nucleus ipsilateral and caudal to the lesion was reduced by approximately 40%. By 21 days, Py-IR was reduced by approximately 50% (a near maximal reduction) and remained constant up to 5 months after the lesion (the longest survival time studied). Alterations of MAP2-IR in Clarke's nucleus were later in onset, slower to develop, and less marked. The differential distribution of the Py antigen in the CNS and its rapid and long lasting loss indicate that the Py antibody is a sensitive tool for studying novel early alterations of the cytoskeleton which may be important molecular events in axotomy-induced pathological processes.
Animals↗
[Subacute encephalopathy with epileptic seizures in a patient with chronic alcoholism (SESA syndrome)].
Subacute encephalopathy with seizures in alcoholics (SESA syndrome) is a rare disease entity following chronic alcohol ingestion. It is quite distinct from alcohol withdrawal syndromes, such as delirium, withdrawal seizures or CNS complications of alcohol, such as Wernicke-Korsakow syndrome, central pontine myelinolysis or Marchiafava-Bignami disease, and was proposed in 1981 by Niedermeyer and coworkers. This syndrome consists of multiple neurological deficits, such as hemiparesis or hemianopia, and of recurrent focal and generalized seizures associated with prominent EEG features (periodic lateralized discharges, PLEDs). A 72-year-old Caucasian male with chronic alcoholism and an otherwise unremarkable past medical history was admitted to our hospital because of several secondary generalized simple partial seizures. Laboratory investigations revealed elevated levels of gamma-glutamyltranspeptidase and of mean corpuscular volume. Other laboratory investigations and the CSF examinations on three occasions revealed normal values. Cranial computed and magnetic resonance tomography showed cerebral microangiopathy and generalized atrophy. Despite triple anticonvulsive therapy and an intravenous treatment with acyclovir and thiamine, the epileptic seizures persisted. Several EEGs revealed left parietooccipital periodic lateralized epileptiform discharges (PLEDs). The patient died of an intercurrent pulmonary infection about 3 months after the onset of symptoms. The described clinical picture resembles the symptoms of SESA syndrome.
Aged↗
Facilitation of picture naming by focal transcranial magnetic stimulation of Wernicke's area.
On the basis of an evolutionary concept of language it was postulated that activation of the motor systems for arm movements, which are phylogenetically older, should facilitate language processes. In aphasic subjects picture naming can be improved by a concomitant movement of the dominant arm. In the present study it was investigated whether a similar facilitation can be observed in normal subjects by studying the effects of transcranial magnetic stimulation (TMS) on picture naming latencies. Suprathreshold focal TMS was applied to the left motor cortex for proximal arm muscles in right-handed subjects. The effects were compared with TMS of Wernicke's area. While TMS of the motor cortex and the non-dominant temporal lobe had no facilitatory effects, TMS of Wernicke's area decreased picture naming latencies significantly when TMS preceded picture presentation by 500 or 1000 ms. The observed effects depended on the intensity of the stimulus used. While clearly present with intensities of 35% and 55% of maximum output the facilitation disappeared with higher stimulation intensities. It is concluded that focal magnetic stimulation is able to facilitate lexical processes due to a general preactivation of language-related neuronal networks when delivered over Wernicke's area.
Adult↗
Distribution of B-50(GAP-43) mRNA and protein in the normal adult human spinal cord.
B-50(GAP-43) is a phosphoprotein mainly found in the nervous system which plays a major role in neurite growth during development and regeneration as well as in synaptic remodelling. In the mature intact central nervous system, intense B-50 immunoreactivity (B-50-IR) can still be detected in regions which maintain residual capacity for structural re-organization. B-50 expression has been studied extensively in laboratory animals; however, its distribution and regulation in the human spinal cord is largely unknown. As a first step to analyze lesion-induced structural alterations, we investigated the distribution of B-50 protein and mRNA in the normal adult human spinal cord and dorsal root ganglia. Intense B-50-IR was localized to the superficial laminae of the dorsal horn at all segmental levels, the intermediolateral nucleus at thoracic levels and Onuf's nucleus at sacral levels. Scattered neurons, particularly in the ventral horn of lumbar and sacral segmental levels (and occasionally also in Clarke's nucleus) displayed intense B-50-IR in close apposition to the perikaryal and proximal dendritic surfaces. Nonradioactive in situ hybridization indicated that B-50 mRNA could also be detected in neurons of the ventral horn and also in the intermediolateral nucleus. The distribution of B-50 mRNA and protein in the normal human spinal cord shows a marked similarity to that reported in experimental animals, including the selective labelling of Onuf's nucleus. However, the strong B-50-IR on the surface of some large anterior horn motor neurons has not been observed in other mammals. This finding might reflect a particular state of readiness for synaptic plasticity.
Aged↗
Interhemispheric inhibition in patients with multiple sclerosis.
OBJECTIVES: A single focal magnetic stimulus applied to the motor cortex of normal subjects can suppress ongoing voluntary electromyographic activity in ipsilateral small hand muscles. This inhibition is mediated from one motor cortex to the contralateral side via a transcallosal pathway. METHODS: We have investigated transcallosal inhibition in 24 patients with definite multiple sclerosis (MS) and in 24 healthy volunteers. A focal magnetic stimulus was applied to the hand area of the motor cortex and the onset latency of the inhibition of the ongoing EMG activity of the ipsilateral first dorsal interosseus muscle was evaluated. Cortico-motor conduction time to the same muscle was revealed, using a magnetic stimulus over the contralateral motor cortex. The difference between these values was calculated as transcallosal conduction time. Cerebral magnetic resonance imaging (MRI) scans including sagittal T2-weighted images were performed in 18 patients. RESULTS: The depth of inhibition (maximal inhibition as percentage of the baseline EMG) in the MS patients was comparable to normal values, but the transcallosal conduction time was significantly delayed (patients 17.2 +/- 6.4 ms; normal subjects 12.2 +/- 2.6 ms; P < 0.001). The duration of the inhibition was significantly prolonged in MS patients (patients 47.9 +/- 20.9 ms; normal subjects 38.9 +/- 10.1 ms; P = 0.02). Transcallosal conduction time was delayed in 11 (46%) of 24 patients, compared with normal subjects. It exceeded the normal range (mean +/- 2.5 SD) in one normal subject (specificity 96%). No correlation could be found between the size or extent of the lesions obtained from the MRI scan and the onset latency or the depth of the inhibition. CONCLUSIONS: We conclude that conduction over transcallosal connections is significantly slower in patients with MS.
Adult↗