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At least 1,243 records · Page 69Linked to original sources
PubMed2005

Subacute inflammatory demyelinating polyneuropathy in children.

Reported are five children with subacute demyelinating polyneuropathy. All patients had a monophasic disease, progressing over 4 to 8 weeks and characterized by predominantly motor features, areflexia, minimal or no cranial nerve abnormalities, no autonomic or respiratory involvement, elevated CSF protein, electrophysiologic evidence of demyelination, and good response to corticosteroids. A benign course with full recovery was the rule.

Adolescent↗
PubMed2001

The pathophysiology of tremor.

Tremor is defined as rhythmic oscillatory activity of body parts. Four physiological basic mechanisms for such oscillatory activity have been described: mechanical oscillations; oscillations based on reflexes; oscillations due to central neuronal pacemakers; and oscillations because of disturbed feedforward or feedback loops. New methodological approaches with animal models, positron emission tomography, and mathematical analysis of electromyographic and electroencephalographic signals have provided new insights into the mechanisms underlying specific forms of tremor. Physiological tremor is due to mechanical and central components. Psychogenic tremor is considered to depend on a clonus mechanism and is thus believed to be mediated by reflex mechanisms. Symptomatic palatal tremor is most likely due to rhythmic activity of the inferior olive, and there is much evidence that essential tremor is also generated within the olivocerebellar circuits. Orthostatic tremor is likely to originate in hitherto unidentified brainstem nuclei. Rest tremor of Parkinson's disease is probably generated in the basal ganglia loop, and dystonic tremor may also originate within the basal ganglia. Cerebellar tremor is at least in part caused by a disturbance of the cerebellar feedforward control of voluntary movements, and Holmes' tremor is due to the combination of the mechanisms producing parkinsonian and cerebellar tremor. Neuropathic tremor is believed to be caused by abnormally functioning reflex pathways and a wide variety of causes underlies toxic and drug-induced tremors. The understanding of the pathophysiology of tremor has made significant progress but many hypotheses are not yet based on sufficient data. Modern neurology needs to develop and test such hypotheses, because this is the only way to develop rational medical and surgical therapies.

Animals↗
PubMed1985

Eye-movement abnormalities in ophthalmoplegia, ataxia, and areflexia (Fisher's syndrome).

Ophthalmoplegia, ataxia, and areflexia are present in a distinctive syndrome called Fisher's syndrome. Eye-movement recordings were used to analyze ophthalmoplegia and other eye-movement abnormalities in three patients. Disorders of supranuclear ocular motor pathways (palsy of upward gaze and internuclear ophthalmoplegia) and peripheral cranial nerve palsies could account for the ophthalmoplegia. In one patient, computed tomography demonstrated a lucency in the midbrain that could be correlated with palsy of upward gaze and bilateral internuclear ophthalmoplegia. Eye-movement abnormalities characteristic of lesions of the midline structures of the cerebellum were documented in two patients. A review of reported cases of Fisher's syndrome and brain-stem encephalitis suggested that these syndromes comprise a spectrum of a reversible, parainfectious process affecting the peripheral cranial nerves and CNS.

Adolescent↗
PubMed1991

Recurrent Fisher's syndrome with immunological abnormalities and replicated laterality.

A case of Fisher's syndrome which recurred 10 years apart was reported. Laterality of cranial nerve findings in the initial episode was replicated in the recurrence. Some kind of localized immune sensitization is supposed to play a role in replicating such a laterality. Increased CD4/CD8 ratio and elevated IgE were noted, which suggests immunological behavior in Fisher's syndrome similar to that in Guillain-Barré syndrome.

Ataxia↗
PubMed2004

[Electroretinogram and electrooculogram in a family with Stargardt's disease].

PURPOSE: The aim of this study is to present the earliest functional changes in Stargardt disease in family with three affected and one unaffected children. PATIENTS AND METHODS: Four children: three girls (4, 7, 10, year old) and one boy (13 year old) and their parents (34 rear old mother and 36 year old father) were examined. Visual acuity (Snellen card), color perception (Ishihara's cards), electroretinography (flash full-field ERG--standard and chromatic) and electrooculography (EOG) were done. For ERG and EOG LKC equipment and UTAS E-2000 program was used. RESULTS: 13 year old boy has had visual acuity about 5/50 for about 3 years, nystagmus and no color perception. On his ocular fundus abnormal macular reflex (like beaten metal) was seen. Visual acuity about 5/12 was found in 7 year old girl during routine examination at school, but color perception and ocular fundus were normal. The others examined family members had visual acuity 5/5 without correction and no changes on ocular fundus. Color perception was normal in girls and mother. The father had red-green deficiency. Arden ratio in EOG was below normal (1.4) only in boy but dark trough and light peak amplitudes were lower than normal also in girls 4 and 7 year old and these two girls were also suspected of Stargardt's disease. ERG was nearly abolished in boy and markedly abnormal in his 7 year old sister. In father's ERG small reduction of cone function especially after chromatic stimulations was found. ERG was normal and similar in mother and 10 year old daughter. ERG was not done in the youngest girl. Two years later loss of visual acuity to 4/50 occurred in girl previously 7 and to 5/6 in the youngest sister. CONCLUSION: Detail analysis of EOG and ERG results may lead to diagnose retinal dystrophy in preclinical stadium.

Adolescent↗
PubMed1977

An investigation into reading epilepsy.

In summary, our main findings were firstly, that faulty visuolingual processing at the level of Brain's visual word schemas, with its intimate connection with the verbal memory pool, is the abnormality that is essential for initiation of spike activity in reading epilepsy. Secondly, visual input is not essential in production of reading epilepsy. Thirdly, we have demonstrated a subconscious voluntary control mechanism operating in our patient. Lastly, we have illustrated alternatives to drug therapy, which, in our patient and in other cases, has not been shown of great value.

Adult↗
PubMed2004

Differential effects of various treatment combinations on cardiovascular dysfunction in patients with Parkinson's disease.

OBJECTIVES: Patients with Parkinson's disease (PD) frequently suffer from cardiovascular dysfunction, which may be enhanced to various extents by different antiparkinsonian drugs. MATERIALS AND METHODS: We analysed electrocardiogram (ECG) abnormalities, cardiovascular reflexes (CVR) and orthostatic hypotension (OH) in 148 patients with idiopathic PD assigned to five different combination therapies of levodopa (LD) plus either bromocriptine (BRO), ropinirole (ROP), selegiline (SEL), anticholinergic (ACH) or amantadine (AMA) or to LD monotherapy before and after a 1-week washout of the add-on drug. Patients were matched for age and disease severity (Hoehn and Yahr stage 2-3). Rater-blinded cardiovascular testing was performed at baseline, and following a 1-week washout period of the add-on drugs. RESULTS: We found that the incidence of cardiovascular dysfunction was generally higher in patients receiving a combination therapy compared with patients on LD monotherapy. ECG abnormalities were found in 40-52% of patients in combination therapy, but in only 20% of the patients receiving LD monotherapy. After discontinuation of BRO and SEL, there were significant improvements in ECG, OH and CVR. After washout of ACH and AMA, a significant improvement was found only in the CVR score. AMA and ROP were the add-on drugs with the least adverse cardiovascular effects. CONCLUSION: We conclude that pre-existing cardiovascular autonomic dysfunction should be investigated and taken into account when deciding which combination therapy to choose in the treatment of parkinsonian patients.

Aged↗
PubMedDate not supplied

[Changes in the cardiovascular chemo-baroreceptors as a possible basis for sudden infant death (SIDS)].

A male sixty days old infant, dying suddenly, has been diagnosed as sudden infant death syndrome (SIDS). Autopsy visualized plurifocal haematic suffusions, typical for an asphyxial status. Abnormalities were not found in the conduction system, but aorticopulmonary paraganglia hyperplasia with mild inflammatory characters has been noted. The role of aorticopulmonary paraganglia, as baro-chemoreceptors, in the cardiovascular regulation, has been anatomical substrate for explaining a sudden infant death, according to a multifactorial theory of SIDS.

Arrhythmias, Cardiac↗
PubMed1978

Autonomic dysfunction in the Landry-Guillain-Barre syndrome.

Tests of autonomic function have been performed on 7 patients with the Landry-Guillain-Barre syndrome and 5 control subjects. These included a sweat test, and measurement of both postural hypotension and baroreflex sensitivity. Sweating was definitely abnormal in 5 patients. Postural hypotension was present in 4 patients. The baroreflex sensitivity was significantly reduced (p less than 0.01) in the patients when compared with the control group. The results demonstrate that both the sympathetic and parasympathetic nervous systems may be affected in the Landry-Guillain-Barre syndrome.

Adult↗
PubMed1983

Quantitative analysis of stance in ataxic myxoedema.

Postural abnormalities in a 66-year-old woman with ataxic myxoedema were recorded by stabilography during treatment. After replacement therapy, 3 Hz power in the sagittal plane was greater than before treatment; this peak shifted to a higher frequency and finally its ratio became normal. This is the first report of recovery of a 3 Hz body oscillation in ataxic myxoedema.

Aged↗
PubMed1992

Long-term outcome in symptomatic carotid sinus hypersensitivity.

Between 1982 and 1988, we observed 312 patients who were affected by syncope or presyncope and whose spontaneous symptoms could be reproduced by means of carotid sinus massage (CSH); no other definite cause of syncope could be identified. The clinical outcome during a 2- to 8-year follow-up period (mean 44 +/- 24 months) was assessed in 262 of them (mean age, 71 +/- 11 years; 183 men) and was compared with that of a group of 55 patients who were affected by unexplained syncope (control patients) who were matched 4:1 for age and sex with CSH patients. CSH patients had an overall mortality rate of 7.3 per 100 person-years (cardiovascular, 66%; sudden death, 9%); overall predicted cumulative survival rates at 1, 3, 5, and 7 years were 92%, 80%, 66% and 53%. Survival was similar in control patients; mortality rate was 5.8 per 100 person-years (cardiovascular, 82%; sudden death, 18%); cumulative survival rates at 1, 3, 5, and 7 years were 85%, 80%, 73%, and 69%. Standardized mortality rate of the general population with similar age and sex distribution, as calculated by means of Italian Istituto Centrale di Statistica death-rate data (1987 edition) was 8 per 100 person-years. Of 13 clinical variables, age, sex, abnormal electrocardiogram, and heart failure (but not CSH type or related arrhythmias) were independently linked to mortality in CSH patients (Cox model). In the vasodepressor form of CSH, patients were younger than those with other forms of CSH and the percentage of women was higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

The flexor carpi radialis H-reflex in polyneuropathy: relations to conduction velocities of the median nerve and the soleus H-reflex latency.

In 80 controls latencies of flexor carpi radialis (FCR) and in 94 controls latencies of soleus H-reflexes correlated well with length of the extremity, body height and age. Multiple regression equations using latency as a variable dependent on age and body height can be best used in practice when both reflexes are employed for demonstration of proximal pathology. The majority (69%) of 93 patients with various polyneuropathies showed abnormalities in both reflexes illustrating that proximal nerve segments are frequently involved. Four per cent had abnormal FCR H-reflexes with normal soleus H-reflexes whereas the reverse was found in 19% of the patients. Abnormal FCR H-reflexes occurred with normal motor and sensory conduction velocities in the peripheral part of the median nerve in 14%, whereas the reverse was seen in 12%, indicating that FCR H-reflex examination is a valuable supplement to conventional conduction studies for detection of electrophysiologically existing pathology.

Action Potentials↗
PubMedDate not supplied

[The Miller Fisher syndrome. Review of the cases of the Santa Maria Hospital].

A benign syndrome of acute ophthalmoplegia, ataxia, and areflexia is commonly known as the Miller Fisher syndrome. It is generally believed that Miller Fisher syndrome is a type of Guillain-Barré syndrome, but several authors believe it to be a separate clinical entity caused by a central nervous system lesion. Eight patients with Miller Fisher syndrome diagnosis, admitted to our department in the last 20 years, were reviewed. Neurophysiological studies were carefully reviewed. Our patients had a clinical presentation and evolution identical to that described previously. Neurophysiological abnormalities were found in all patients and were characteristic of a sensory axonal neuropathy, with damage of the facial nerves and occasional demyelination of peripheral nerves. The pattern of abnormalities is distinct from the usual features seen in Guillain-Barré syndrome. The CT scan, MRI, and Evoked Potentials investigations in our patients did not confirm central nervous system lesion. Nevertheless we did not exclude the possibility of coexisting damage to the central nervous system in some patients, as shown in Chronic Inflammatory Demyelinating Polyneuropathy.

Adult↗
PubMed1999

An infection-based model of neurodevelopmental damage.

Perinatal exposure to infectious agents and toxins is linked to the pathogenesis of neuropsychiatric disorders, but the mechanisms by which environmental triggers interact with developing immune and neural elements to create neurodevelopmental disturbances are poorly understood. We describe a model for investigating disorders of central nervous system development based on neonatal rat infection with Borna disease virus, a neurotropic noncytolytic RNA virus. Infection results in abnormal righting reflexes, hyperactivity, inhibition of open-field exploration, and stereotypic behaviors. Architecture is markedly disrupted in hippocampus and cerebellum, with reduction in granule and Purkinje cell numbers. Neurons are lost predominantly by apoptosis, as supported by increased mRNA levels for pro-apoptotic products (Fas, caspase-1), decreased mRNA levels for the anti-apoptotic bcl-x, and in situ labeling of fragmented DNA. Although inflammatory infiltrates are observed transiently in frontal cortex, glial activation (microgliosis > astrocytosis) is prominent throughout the brain and persists for several weeks in concert with increased levels of proinflammatory cytokine mRNAs (interleukins 1alpha, 1beta, and 6 and tumor necrosis factor alpha) and progressive hippocampal and cerebellar damage. The resemblance of these functional and neuropathologic abnormalities to human neurodevelopmental disorders suggests the utility of this model for defining cellular, biochemical, histologic, and functional outcomes of interactions of environmental influences with the developing central nervous system.

Animals↗
PubMed1988

Reversible alterations of cerebral gamma-aminobutyric acid in pyrithiamine-treated rats: implications for the pathogenesis of Wernicke's encephalopathy.

Treatment of rats with the central thiamine antagonist, pyrithiamine, results in severe neurological symptoms such as loss of righting reflex. Measurement of gamma-aminobutyric acid (GABA) content of brain tissue from symptomatic pyrithiamine-treated (PT) rats revealed significant reductions in thalamus, cerebellum, and pons. GABA content of cerebral cortex, however, was unaltered. Activities of the thiamine-dependent enzyme alpha-ketoglutarate dehydrogenase (alpha KGDH) were reduced in parallel with the GABA changes. On the other hand, activities of the GABA-synthetic enzyme glutamic acid decarboxylase (GAD) remained within normal limits, with the exception of a small but significant decrease in thalamus of symptomatic PT rats. Affinities and densities of high-affinity [3H]muscimol binding sites on crude cerebral membrane preparations from symptomatic PT rats were unchanged. Thiamine administration to symptomatic animals resulted in correction of abnormal righting reflexes and in normalization of decreased GABA levels and reduced alpha KGDH activities in cerebellum and pons. Thalamic GABA levels and alpha KGDH activities, on the other hand, remained significantly lower than normal. These results suggest that the reversible symptoms of pyrithiamine treatment may result from imparied GABA synthesis in cerebellum and pons of these animals. Similar mechanisms may play a role in the pathogenesis of the reversible symptoms of Wernicke's encephalopathy in man.

Animals↗
PubMed1998

Neurotoxicity of isolated limb perfusion with tumor necrosis factor.

Hyperthermic isolated limb perfusion (HILP) with tumor necrosis factor alpha (TNFalpha) is effective for advanced melanoma and sarcoma of the limbs. Ten patients undergoing HILP with TNFalpha were evaluated by neurological examinations, nerve conduction studies (NCS), sympathetic skin responses (SSR) and conventional and quantitative electromyography (EMG), performed before, 7 days and 6 weeks following HILP. Seven patients showed minimal clinical signs of peripheral nerve damage following HILP; in two the injury was evident electrophysiologically: 7 days following HILP five patients had paresthesias and/or hypoesthesia, one had a mild foot drop and one had autonomic disturbances in the affected limb. SSR was low in two patients in the affected limb, sensory nerve action potentials were not elicited in one, with normal motor NCS and EMG. At 6 weeks, four patients continued to have mild paresthesias and one had dysautonomia of the perfused limb. Sensory responses and SSR did not change, motor abnormalities were not found. These findings show that HILP with TNFalpha induces a mild, mainly sensory neuropathy in perfused limbs, not disturbing functionality and improving over time.

Adult↗
PubMed1995

Randomized perturbed posturography in abstinent chronic alcoholics.

Equilibrium is maintained by visual, proprioceptive and vestibular afferent influx, central coordination and motor efferents. Eleven male abstinent chronic alcoholic volunteers aged 44-65 years (mean 57 years) were investigated by randomized perturbed posturography. They had all been long time heavy drinkers. Ocular smooth pursuit and visual suppression of the vestibulo-ocular reflex showed abnormalities in a previous study, but they had no signs or symptoms of polyneuropathy. The current study demonstrated larger (but generally not significantly so) sway areas, and in all tests on the randomly moving support surface the sway velocities were significantly larger than in the controls. It is concluded that randomized perturbed posturography is valuable in dysequilibrium assessment in chronic alcoholics.

Adult↗
PubMed1986

Computerized tomographic abnormalities in patients with hemispheric transient ischemic attacks.

In 100 patients with transient ischemic attacks, correlations between clinical features and CT findings were analyzed. In 77 patients, CT scans were normal. Five percent had mass lesions and 18 had vascular lesions (ischemia, infarction, hematoma) delineated by CT. In two patients whose CT showed a hypodense lesion indicating cerebral infarction, clinical and CT worsening followed carotid surgery. In six patients with isodense enhancing lesions indicating ischemia, there was no clinical or CT deterioration after operation.

Adult↗