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Biomedical subjects

J Noth

Publications and source records attributed to J Noth.

At least 19 recordsLinked to original sources
PubMed1992

Abnormalities of somatosensory evoked potentials in the quinolinic acid model of Huntington's disease: evidence that basal ganglia modulate sensory cortical input.

Intrastriatal injection of quinolinic acid (QA) in rats provides an animal model that mimics some of the neuropathological and neurochemical alterations observed in the striatum of patients with Huntington's disease (HD). One of the very early neurophysiological signs in HD is a diminution of amplitude of early somatosensory evoked potentials (SEPs) recorded over the parietal cortex. The present study investigated whether the QA model exhibits similar neurophysiological abnormalities. Two weeks after unilateral intrastriatal injection of QA (240 nmol) or of the solvent, early SEPs were recorded with chronically implanted electrodes from the somatosensory cortex or from the ventrobasal nucleus of the thalamus of lightly pentobarbital-anesthetized rats, in response to single-shock electrical stimulation of the contralateral forepaw. Whereas intrastriatal injection of solvent did not influence SEPs, the striatal QA lesion significantly reduced the amplitude of early cortical SEPs by about 40% without affecting the latency. SEPs recorded from the ventrobasal nucleus were unchanged after QA lesion. Histological examination and glial fibrillary acid protein staining after intrastriatal injection of QA revealed no evidence for damage in the somatosensory system. It is concluded that (1) the QA animal model of HD mimics some of the SEP abnormalities of patients, and (2) a striatal lesion modulates somatosensory transmission to the cortex in rats.

Animals↗
PubMed1992

Contralateral early blink reflex in patients with facial nerve palsy: indication for synaptic reorganization in the facial nucleus during regeneration.

Fifty patients with Bell's palsy and 30 patients with etiologically different symptomatic peripheral facial nerve palsy were studied by means of electrically evoked blink reflexes 1-23 days after onset of paresis. Their results were compared with a normal control group of 30 healthy subjects. In a significant number of patients (64% in Bell's palsy and 53% in symptomatic facial nerve palsy) a contralateral early blink reflex response (R1) could be elicited upon stimulation of the normal side as compared to 13% in the control group. It is suggested that this result may be explained by synaptic reorganization of the facial nucleus leading to functional unmasking of pre-existing crossed trigemino-facial reflex pathways during regeneration. This view is in line with previous experimental data in animals on the time course of structural changes in the facial nucleus after lesioning of the ipsilateral facial nerve.

Adolescent↗
PubMed1992

Motor responses evoked by magnetic brain stimulation in Huntington's disease.

In 34 patients with manifest Huntington's disease (HD), and in 21 first-degree offspring without clinical signs or symptoms, the sizes, central motor latencies (CMLs) and variation in latencies of EMG responses (MEPs) following transcranial magnetic brain stimulation were studied in muscles of the upper and lower extremities. In subgroups of patients and their offspring median and tibial nerve somatosensory evoked potentials (SEPs) and electrically elicited long-loop reflexes (LLRs) in hand muscles were also investigated. Increased MEP thresholds were observed in 10% of the HD offspring, while CML, latency variability and MEP amplitudes always lay within normal range. In contrast, SEPs were abnormal in 33%. In HD patients MEPs were found to be abnormal in up to 72% of patients when all available response parameters were taken into consideration. MEP abnormalities correlated with the duration of motor symptoms and the severity of choreic motor activity. When both MEPs and SEPs were evaluated, abnormalities could be detected in 91% of all HD patients. We suggest that abnormal MEPs might reflect an altered excitability of the cortico-spinal system as a consequence of basal ganglia dysfunction, rather than a structural damage of the investigated descending pathways. To localize the pathological mechanism responsible for altered LLRs, a "loop analysis" was performed by recording LLRs, MEPs and SEPs in the same patients. Alterations of LLRs correlated best with abnormal SEPs and might therefore be explained by reduced somatosensory input to the motor cortex.

Adolescent↗
PubMed1991

Trends in the pathophysiology and pharmacotherapy of spasticity.

Spasticity develops after supraspinal or spinal lesions of descending motor systems, with obligate involvement of the corticospinal tract. Spasticity is characterized by an increase in muscle tone, which, in contrast to many other types of enhanced muscle tone, shows a marked velocity-dependent increase when the muscle is passively stretched. The pathophysiological mechanisms underlying this spastic muscle tone remain obscure. Three major causes are currently considered possible: (1) changes in the excitability of spinal interneurones; (2) receptor hypersensitivity; (3) formation of new synapses by sprouting. The latter mechanism could account for the long time course over which spastic muscle tone develops in hemiplegic or paraplegic patients, but there is no experimental evidence for this hypothesis. The electromyographic (EMG) gait analysis of patients with spasticity has thrown doubt on the common belief that the velocity-dependent increase in spastic muscle tone is evoked by stretch reflex activity and has led to the idea that spastic muscle tone resides in the muscle fibres themselves. While such a mechanism may contribute to the slowness of active movements in spastic patients, recent experiments on patients with spastic arm paresis have confirmed the classical view that the spastic muscle tone is related to the EMG activity evoked in the passively stretched muscle. This pathological EMG activity is seen during the entire range of the dynamic phase of the stretch, during which a normal muscle exhibits only an early, phasic burst at the highest stretch velocities employed. For the pharmacological treatment of spasticity, substances with different central or peripheral actions are available. Their assumed receptor actions are described, together with their main indications and side-effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Electromyography↗
PubMed1991

Language functions in progressive supranuclear palsy.

Language functions were studied in 6 patients with clinically diagnosed progressive supranuclear palsy who conformed to the characteristic pattern of 'subcortical dementia'. Dysarthria, reading difficulties and disturbances of handwriting were present in all patients. Some patients showed additional deficits including visual dyslexia, constructional dysgraphia and an increased rate of self-corrections and misnamings in object confrontation naming. In most instances, the naming errors referred to an object visually similar to the target object, suggesting that visual misperception is the major cause of the naming disorder. It is concluded that a variety of language impairments may develop secondary to other neurological and neuropsychological changes in progressive supranuclear palsy.

Aged↗
PubMed1991

Different mechanisms underlie the long-latency stretch reflex response of active human muscle at different joints.

1. Stretch of voluntarily activated human muscle results in a reflex response consisting of short-latency (M1) and delayed long-latency (M2) components. The mechanism of the M2 response remains the subject of controversy. The present study tested the universality of the hypothesis that the M2 response results from the transmission of low-threshold muscle afferent input travelling over a long-loop supraspinal pathway. Muscle reflex responses resulting from imposed stretch were obtained from the first dorsal interosseus (FDI), biceps brachii (BB), triceps brachii (TB) and triceps surae (TS) muscles. 2. Patients suffering from Huntington's disease (HD) show a selective loss of FDI-M2 responses, with sparing of the M1. This has been attributed to disruption of supraspinal pathways as a part of the disease pathology. Accordingly, HD has been used in the present study as a model to test the universality of the long-loop hypothesis: if this is so, then HD patients with an absent FDI M2 should also fail to show an M2 response in other muscles. 3. It is shown that a group of HD patients in whom the FDI-M2 response was absent or residual developed clear M2 responses in the TB, BB and TS muscles following stretch sufficient to invariably evoke this component in normal subjects. 4. It is thus concluded that longer-latency stretch reflex components are not invariably mediated over long-loop supraspinal pathways, but that this mode of control is dominant only in muscles, such as those of the hand, whose function depends largely on direct cortical control.

Adult↗
PubMed1991

Evidence that low-threshold muscle afferents evoke long-latency stretch reflexes in human hand muscles.

1. The aim of the present study was to identify the type of spinal afferents involved in the generation of the long-latency response in intrinsic human hand muscles. Position-controlled extensions were imposed on the index finger or on the wrist of healthy subjects who were exerting a steady voluntary flexion force at the relevant joint. Averaged surface electromyographic (EMG) responses of the first dorsal interosseus muscle (FDI) or of the wrist flexors were evaluated with respect to latency and size. 2. Small transient angular displacements of the index finger (1 degree, as measured at the metacarpophalangeal joint), which are supposed to excite primary rather than secondary afferents, evoked two clearly discernible EMG responses with mean latencies of 32.3 ms (M1 response) and 54.7 ms (M2 response), respectively. The size of the M2 response exceeded the size of the M1 response by 60%. In the wrist flexors, transient stretch (1 degree) gave rise to a large M1 response (latency 22.8 ms) and a small, inconstent M2 response. 3. Small-amplitude vibration of the index finger elicited EMG responses in the FDI that were qualitatively and quantitatively similar to those seen in response to small transient stretches of the index finger. This was also true for fast ramp-and-hold stretches (stretch velocity 400 degrees/s, amplitude 5 degrees), whereas slow ramp-and-hold stretches (125 degrees/s, 5 degrees) elicited predominantly M2 responses. 4. In the FDI, the mechanical threshold of the M1 and M2 response to the transient angular displacement was approximately 0.15 degrees, with a tendency for the M2 response to appear at a lower threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Musical hallucinations in hearing loss in the aged].

An 83-year-old woman experienced the abrupt onset of musical hallucinations. She had had long-standing progressive hearing loss due to otosclerosis. The clinical, psychopathological and pathogenetic aspects of this syndrome are discussed by means of a review of the literature.

Aged↗
PubMed1990

[Neurologic and psychiatric disorders in vinyl chloride disease].

A literature review and an own case observation of neurological and psychiatrical disturbances in vinyl chloride disease are presented. In acute vinyl chloride intoxication, patients complain of vertigo, nausea and headache. At higher concentrations, vinyl chloride exerts a narcotic effect. In patients with chronic occupational exposure, neurological disturbances include sensory-motor polyneuropathy, trigeminal sensory neuropathy, slight pyramidal signs and cerebellar and extrapyramidal motor disorders. Psychiatric disturbances present as neurasthenic or depressive syndromes. Sleep disorders and disorders of sexual functions are frequently encountered. Pathological EEG alterations can be found in a high proportion of patients. The long term course and prognosis of the neurological and psychiatrical disorders in vinyl chloride disease are obscure. In an own case, a slight sensory polyneuropathy, bilateral hyposmia, a marked neurasthenic syndrome, typical EEG changes and computed tomography signs of cerebral atrophy were found in a 56-years-old patient as late as 16 years after the exposure to vinyl chloride.

Adult↗
PubMed1989

[The Charles Bonnet syndrome].

The Charles Bonnet syndrome represents an organic hallucinosis characterized by the appearance of visual hallucinations in otherwise sane elderly people. As a specific organic factor, a reduced visual acuity due to ophthalmologic disorder can be found in the majority of patients. Clinical, psychopathological and pathogenetic aspects of the Charles Bonnet syndrome are discussed by the means of a review of 46 cases reported in the literature (including an own case observation).

Aged↗
PubMed1989

Achromobacter xylosoxidans corneal ulcer in a therapeutic soft contact lens wearer.

Achromobacter xylosoxidans is an opportunistic organism that is usually seen in immunocompromised or immunosuppressed patients. It is an aerobic gram-negative rod, often confused with other more commonly seen gram-negative bacteria such as Pseudomonas aeruginosa. The organism is usually sensitive to extended spectrum penicillins such as carbenicillin and usually resistant to aminoglycosides and first generation cephalosporins. We wish to describe a corneal ulcer from A. xylosoxidans that developed in a patient wearing a therapeutic soft contact lens. The patient did not have a preexisting microbial keratitis and was not receiving corticosteroid therapy.

Aged↗
PubMed1988

Reconsideration of the concept of enhanced static fusimotor drive in rigidity in patients with Parkinson's disease.

The electromyographic responses elicited in the first dorsal interosseus muscle by small muscle stretches or by electrical stimulation of the median nerve were investigated in parkinsonian patients and in age-matched healthy subjects. Stimuli were applied during a steady level of contraction in the intrinsic hand muscle. This ensured comparable levels of excitability in the alpha-motoneurone pool in patients and normals. It was found that the normal short-latency stretch reflex was almost absent in rigid patients, while responses to electrical stimulation of low-threshold nerve fibres were of equal size in both groups. This result suggests that there is a change in fusimotor control of muscle spindles in Parkinson's rigidity without alteration of the central gain of the Ia-transmitted stretch reflex.

Electric Stimulation↗
PubMed1988

Language functions in Huntington's disease.

A comprehensive language test battery (Aachen Aphasia Test) was administered to 45 patients in the early, middle or later stages of Huntington's disease (HD) and to 20 control subjects. In spontaneous speech, many HD patients exhibited a loss of conversational initiative. Dysarthria was a common finding. Reading skills were found to be impaired mainly as a consequence of dysarthria; some HD patients displayed visual dyslexia. In addition to the characteristic disturbances of writing skills due to the choreiform movement disorder, the writing of HD patients with advanced dementia indicated constructional dysgraphia, characterized by frequent omissions, perseverations and substitutions. HD patients exhibited no evidence of word-finding difficulty or other semantic deficits in spontaneous speech. There was, however, a marked impairment in visual confrontation naming, with a significant rise in naming error rate as the disease progressed in severity. In most instances, the inappropriate names referred to an object visually similar to the target object, suggesting that visual misperception is the major cause of the naming disorder in HD. Syntactical structure of spontaneous speech was typically reduced to short, simple sentence construction. Verbal stereotypes were only rarely encountered and occurred late in the course of the disease. Tests of language comprehension reflected the general degree of dementia. It is concluded that there are no primary language changes in HD. Instead, a variety of language impairments develop secondary to other neurological and neuropsychological changes.

Adult↗
PubMed1987

Medium and long latency EMG responses in leg muscles: Parkinson's disease.

Short, medium, and long latency EMG responses to muscle stretch from triceps surae and anterior tibialis muscles were recorded in normals and in 33 patients with Parkinson's disease. The latencies of all EMG responses except short latency were normal in patients with Parkinson's disease. The integrals of the medium latency responses in the stretched triceps surae muscle were significantly increased in patients. This result indicates a modulatory influence of the basal ganglia on medium latency EMG responses.

Adult↗