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PubMed1964

STRABISMUS IN GENERAL PRACTICE.

Considerable confusion exists concerning the time at which a cross-eyed child should be referred to an ophthalmologist. This referral should be made between six and nine months because visual and muscular coordinated reflexes necessary for normal vision and stereopsis develop at six months, and 80% of these reflexes are established by the age of two. Normal anatomical relations must be established shortly after six months to avoid the formation of fixed, irreversible, abnormal reflexes which lead to loss of vision in one eye and lack of stereopsis.The recommended classification of crossed eyes emphasizes the insidious divergent type that must be treated in infancy.Reasons for delay in referring cross-eyed children include incorrect advice from the family doctor and inappropriate advice from optometrists. Treatment is aimed at the development of normal vision in each eye, stereopsis, and a good cosmetic result.

Adolescent↗

PubMed1995

Nerve injury in adult rats causes abnormalities in the motoneuron dendritic field that differ from those seen following neonatal nerve injury.

Disruption of neuromuscular contact by nerve-crush during the early postnatal period causes increased activity and abnormal reflex responses in affected motoneurons, but such changes are not found after nerve-crush in adult animals. We found previously that neonatally lesioned cells develop an abnormal dendritic field, which may explain the functional changes. Here we have studied the dendritic morphology of the same motoneuron pool after nerve-crush at maturity in order to correlate the observed alterations in morphology with physiological findings. One to two months after sciatic nerve-crush in adult animals, motoneurons supplying the extensor hallucis longus muscles of the rat were retrogradely labelled with cholera toxin subunit-B conjugated to horseradish peroxidase. The dendritic tree of labelled cells was then analysed. Following adult nerve-crush, the dendritic tree of the motoneurons was smaller but did not display the localised increase in dendritic density seen after neonatal nerve-crush. These findings support the view that such specific morphological changes contribute to the physiological abnormalities seen only after neonatal nerve injury.

Animals↗

PubMed1992

Are medium and long latency reflexes a screening tool for early Parkinson's disease?

We have studied whether assessment of medium latency (ML) and long latency (LL) reflex amplitudes may serve as a marker for early Parkinson's disease. Twenty-three patients with idiopathic Parkinson's disease (Hoehn and Yahr stage 1 to 4) and 24 controls received 20 4 degrees toe-up rotations of a platform upon which they were standing. All antiparkinsonian medication was withheld for at least 12 h before the study. ML reflexes in the stretched gastrocnemius muscle and LL reflexes in the shortened tibialis anterior muscle were recorded from both legs. ML responses were significantly enhanced in patients compared to controls. In contrast to previous studies which studied patients who continued their usual treatment, we observed that LL responses were significantly reduced in patients compared to controls. For the purpose of individual analysis, we subsequently determined the optimal specificity and sensitivity using various criteria for abnormality. The presence of either enhanced ML responses or reduced LL responses (or both) in at least one leg yielded a maximum sensitivity of 65.2% with a specificity of 75.0% (positive likelihood ratio 2.6; negative likelihood ratio 0.5). Abnormal reflexes were almost exclusively present in patients with advanced and long-standing Parkinson's disease. These results show abnormalities of ML and LL responses in advanced Parkinson's disease, but render it unlikely that these abnormalities are a suitable screening tool for early stages of the disease. The fact that LL responses were reduced in patients taken off antiparkinsonian medication raises the possibility that this reflex is under supraspinal dopaminergic control.

Aged↗

PubMed1981

Heart rate changes in diabetes mellitus.

Resting heart rates were measured lying, sitting, and standing in 61 diabetics with varying degrees of cardiovascular reflex abnormalities. Those with parasympathetic abnormalities alone had the highest heart rates, while those with both parasympathetic and sympathetic involvement had slightly less rapid heart rates, which were still faster than those in diabetics with normal cardiovascular reflexes. 38 other diabetics in whom autonomic function tests had been done at least three times had a similar pattern of resting heart rate. 25 had unchanged tests: those with parasympathetic involvement alone had the highest heart rates. The other 13 subjects whose autonomic function changed from normal to abnormal showed a sequential increase in heart rate as cardiac parasympathetic damage developed, followed by a fall in heart rate, but not back to normal, as sympathetic damage developed as well. The increased resting heart rates in diabetics may be due in some patients to cardiac parasympathetic damage alone and in others to combined parasympathetic and cardiac sympathetic damage. The sequential heart rate changes support the view that the vagus nerve is affected before the cardiac sympathetic nerves.

Adolescent↗

PubMed2005

Abnormal forebrain activity in functional bowel disorder patients with chronic pain.

BACKGROUND: Abnormal cortical pain responses in patients with fibromyalgia and conversion disorder raise the possibility of a neurobiologic basis underlying so-called "functional" chronic pain. OBJECTIVE: To use percept-related fMRI to test the hypothesis that patients with a painful functional bowel disorder do not process visceral input or sensations normally or effectively at the cortical level. METHODS: Eleven healthy subjects and nine patients with irritable bowel syndrome (IBS) underwent fMRI during rectal distensions that elicited either a moderate level of urge to defecate or pain. Subjects continuously rated their rectal stimulus-evoked urge or pain sensations during fMRI acquisition. fMRI data were interrogated for activity related to stimulus presence and to specific sensations. RESULTS: In IBS, abnormal responses associated with rectal-evoked sensations were identified in five brain regions. In primary sensory cortex, there were urge-related responses in the IBS but not control group. In the medial thalamus and hippocampus, there were pain-related responses in the IBS but not control group. However, pronounced urge- and pain-related activations were present in the right anterior insula and the right anterior cingulate cortex in the control group but not the IBS group. CONCLUSIONS: Percept-related fMRI revealed abnormal urge- and pain-related forebrain activity during rectal distension in patients with irritable bowel syndrome (IBS). As visceral stimulation evokes pain and triggers unconscious processes related to homeostasis and reflexes, abnormal brain responses in IBS may reflect the sensory symptoms of rectal pain and hypersensitivity, visceromotor dysfunction, and abnormal interoceptive processing.

Adult↗

PubMed1999

Ocular motor abnormalities in ataxia telangiectasia.

Although abnormal eye movements are a prominent feature of ataxia telangiectasia, the characteristics of the oculomotor dysfunction in the disease have been reported only in small groups of patients. We have examined eye movements clinically in 56 patients with ataxia telangiectasia, and obtained electrooculographic recordings of eye movements in 33 subjects. Deficits were observed in the eye movement systems that stabilize images on the retina, including pursuit, gaze holding, convergence, vestibular and optokinetic slow phases, and cancellation of vestibular slow phases. Abnormalities in the systems that maintain fixation and shift gaze were also prominent, including abnormal reflexive and voluntary saccades (characterized by prolonged latency, hypometric amplitude, and the use of head movements to initiate gaze shifts), impaired fixation, and a reduction in vestibular and optokinetic quick phases. The abnormalities in image stabilization most likely result from dysfunction in the cerebellar flocculus and paraflocculus. The basis of the saccadic and fixation disturbance is less certain but may be the result of abnormal supranuclear control of the superior colliculus resulting from dysfunction in the cerebellar vermis or the basal ganglia.

Adolescent↗

PubMed1996

[Reflex sympathetic dystrophy syndrome associated with phenobarbital].

Reflex sympathetic dystrophy syndrome (RSDS) is clinically characterized by pain and edema of one or more extremities, trophic skin changes and vasomotor instability. Although the pathogenesis is unknown, it could be caused by an abnormal reflex of the sympathetic nervous system. Different studies haven't yet confirmed the classical division in three clinical phases (warm, of vasomotor instability and cold). Barbiturates are the precipitating event in 10-30% of cases. We describe the clinical features of a patient with RSDS associated with phenobarbital who needed corticosteroid treatment. The Technetium diphosphate bone scan (Tc 99m DPD) is very useful because there is an increased radionuclide uptake in the involved areas during the early phases of the disease and precedes in some weeks the radiologic signs. The Magnetic Resonance Imaging (MRI) may be useful because of the early signs it shows. The patient may develop contractures and atrophy of the involved extremities in spite of the indispensable withdrawal of the drug.

Aged↗

PubMed1986

Abnormality of circulatory reflex and aldosterone response during head-up tilting in patients with primary aldosteronism.

Abnormality of the circulatory reflexes has been reported in patients with primary aldosteronism. However, changes in blood pressure, heart rate, plasma renin activity (PRA), and plasma aldosterone concentration (PAC) after head-up tilting in primary aldosteronism have not yet been reported. Seven patients with primary aldosteronism were tilted to a 65 degree head-up position which was maintained for 30 min. Systolic blood pressure decreased significantly 5 min after tilting and remained at this level during the period of tilting. Diastolic blood pressure did not change during the tilting. Heart rate increased after 5 min of tilting and this level of heart rate was maintained for 30 min. Plasma renin activity was low and did not change during tilting. However, plasma aldosterone concentration increased significantly 20 min after tilting. Plasma cortisol concentration and plasma ACTH concentration also increased significantly. These results suggest that primary aldosteronism causes abnormalities of the circulatory reflexes. The increase of endogenous ACTH may increase plasma aldosterone concentration in patients with primary aldosteronism.

Adrenocorticotropic Hormone↗

PubMed1985

Cutaneous reflex responses recorded in children with various neurological disorders.

Cutaneous reflex responses were recorded from tibialis anterior or first dorsal interosseous muscles of children with hemiplegia, spinal-cord compression, necrotizing sacroid granulomatosis, acute encephalomyelitis, myalgic encephalomyelitis, and a group of children attending the Learning Difficulties Clinic. Abnormalities of response are reported and are compared with the different reports in the literature of abnormal reflex EMG responses recorded by various methods. It is concluded that cutaneo-muscular reflex testing may have a part to play in the diagnosis of difficult paediatric problems.

Adolescent↗

PubMed2000

[Pathophysiology of abnormal movements in Parkinson's disease].

Major parkinsonian motor symptoms, i.e., bradykinesia, muscular rigidity, and resting tremor, are due to abnormalities in the motor circuit of the basal ganglia caused by loss of nigrostriatal dopamine neurons. Bradykinesia results from increased activity with altered firing patterns of the output nuclei of the basal ganglia. Exaggerated long-latency reflex or decreased Ib inhibition of the spinal reflex network have been suggested to underlie rigidity, but the relationship between these reflex abnormalities and the altered activities of the basal ganglia in the parkinsonian state remains unclear. The central oscillator for parkinsonian tremor has been localized in the basal ganglia circuit, and the cerebellar system also participates in generation of the tremor. Dyskinesia and dystonia may develop from decreased activity with altered firing patterns of the output nuclei of the basal ganglia.

Animals↗

PubMed1986

Clinical correlates of abnormal P14 in median SEPs.

Recording median somatosensory evoked potentials (SEPs) from scalp and neck in separate channels with the use of an ear reference, 52 patients had abnormal scalp-recorded P14 associated with normal cervical-recorded N13. The patients had multiple sclerosis or other brainstem or high cervical cord lesions. Evidence of brainstem lesions was found in 35 patients on clinical examination or by brainstem auditory evoked potentials or blink reflex. Abnormalities of P14 were correlated highly with brainstem dysfunction, but high cervical cord lesions could not be excluded by this finding. The localizing value of SEP is improved by measuring the N13 and P14 peaks separately and assessing the cervical cord-brainstem conduction time.

Adult↗

PubMed1984

The heart in diabetes.

Since the introduction of insulin, heart disease has become a major impediment to survival in persons with diabetes mellitus. Coronary disease has increased severity and accelerated development in diabetic persons compared with an age- and sex-matched nondiabetic population. A peculiar vulnerability of women to the influence of diabetes with loss of premenopausal coronary disease protection has been found. The symptomatology of coronary events may differ and coronary care data show a higher incidence of sudden death in diabetic patients who have a myocardial infarction than in their non-diabetic counterparts. Insulin may play a role in the myocardial adjustment to an ischemic insult by enhancing glucose intake and suppressing lipolysis and ketogenesis. Carbohydrate intolerance in dogs, rhesus monkeys and humans appears associated with similar histologic and compositional changes in the myocardium. Abnormalities in diastolic ventricular function not attributable to large- or small-vessel coronary disease have been found in the diabetic subjects of each species. Studies in humans who have diabetes have assessed single pressure-volume relationships and more exacting measures of ventricular compliance are needed. Abnormalities of myocardial function in patients with diabetes have been found using echo and radionuclide techniques. Many of these findings need to be correlated with invasive data or confirmed in larger populations. Autonomic dysfunction is common in diabetic persons and may imply an associated poor prognosis. Reflex abnormalities in parasympathetic function are most prevalent and occur before sympathetic dysfunction.

Adult↗

PubMed1998

The pathophysiology of primary dystonia.

Co-contraction and overflow of EMG activity of inappropriate muscles are typical features of all dystonic movements whether voluntary or involuntary. Voluntary movements are slow and more variable than normal, and there is particular difficulty switching between component movements of a complex task. Reduced spinal cord and brainstem inhibition is common to many reflex studies (long-latency reflexes, cranial reflexes and reciprocal inhibition). These reflex abnormalities may contribute to the difficulties in voluntary movements but cannot be causal as they can occur outside the clinically involved territory. Clinical and neurophysiological studies have emphasized the possible role of sensory feedback in the generation of dystonic movements. Abnormalities of cortical and basal ganglia function have been described in functional imaging and neurophysiological studies of patients with dystonia and in animal models of primary dystonia. Studies of cortical function have shown reduced preparatory activity in the EEG before the onset of voluntary movements, whilst magnetic brain stimulation has revealed changes in motor cortical excitability. Functional imaging of the brain in primary dystonia has suggested reduced pallidal inhibition of the thalamus with consequent overactivity of medial and prefrontal cortical areas and underactivity of the primary motor cortex during movements. These findings are supported by preliminary neuronal recordings from the globus pallidus and the thalamus at the time of stereotaxic surgery in patients with dystonia. All this evidence suggests that primary dystonia results from a functional disturbance of the basal ganglia, particularly in the striatal control of the globus pallidus (and substantia nigra pars reticulata). This causes altered thalamic control of cortical motor planning and executive areas, and abnormal regulation of brainstem and spinal cord inhibitory interneuronal mechanisms.

Animals↗

PubMed1988

Increased exercise ventilation in patients with chronic heart failure: intact ventilatory control despite hemodynamic and pulmonary abnormalities.

This study was designed to determine the pathophysiologic basis of increased exercise ventilation in the presence of chronic heart failure. Sixty-four ambulatory patients with chronic heart failure and 38 age-matched normal control subjects performed exercise according to identical staged, symptom-limited bicycle exercise protocols with measurement of hemodynamic, ventilatory, and metabolic responses. Compared with normal subjects, ventilation and the ratio of ventilation to CO2 production (Ve/VCO2), and pulmonary capillary wedge pressure were elevated in patients at rest and during exercise. The ratio of pulmonary dead space to tidal volume (Vd/Vt) also was elevated in the heart failure group at rest and during exercise and was closely related to Ve/VCO2 (all r greater than .72, p less than .001). Rest and exercise arterial PCO2 regulation was normal in patients. Peak exercise Ve/VCO2 did not correlate with pulmonary vascular pressures, but was inversely related to cardiac output (r = -.49, p less than .001). Thus, neurohumoral ventilatory control mechanisms are intact in patients with chronic heart failure and act to maintain normal PaCO2 levels in the face of increased pulmonary dead space. Activation of abnormal reflexes due to hemodynamic derangements during exercise are not important in determining ventilation in the presence of chronic heart failure. The demonstration of a correlation between decreased cardiac output and increased ventilation in the patient group suggests that attenuated pulmonary perfusion may play a role in causing exercise hyperpnea in the presence of chronic heart failure by producing ventilation perfusion abnormalities and thereby increasing physiologic pulmonary dead space.

Exercise Test↗

PubMed1998

Exercise-induced abnormal blood pressure responses are related to subendocardial ischemia in hypertrophic cardiomyopathy.

OBJECTIVES: We examined by thallium-201 scintigraphy whether exercise-induced abnormal blood pressure response (BPR) is related to myocardial ischemia. BACKGROUND: Hemodynamic instabilities during exercise in patients with hypertrophic cardiomyopathy (HCM) are considered to be caused by abnormal reflex control of vascular resistance. METHODS: In 105 patients with HCM, exercise thallium scintigraphy was performed by means of a multistage, symptom-limited bicycle ergometer exercise test. RESULTS: Eighty-eight patients had normal BPR (> or = 25 mm Hg from baseline to peak exercise), and 17 had abnormal BPR (<25 mm Hg). Clinical characteristics including age, the prevalence of obstruction, New York Heart Association functional class and echocardiographic measurements were similar between the two groups. Left ventricular end-diastolic pressure was significantly higher in patients with abnormal BPR than in those with normal BPR (18+/-8 vs. 14+/-5 mm Hg, p < 0.05). Exercise-induced perfusion abnormalities including fixed and reversible perfusion defects, and left ventricular cavity dilatation (LVCD) were identified in 72 (69%) of 105 study patients. Left ventricular cavity dilatation indicates subendocardial hypoperfusion and is a marker of diffuse subendocardial ischemia. The prevalence of fixed or reversible perfusion defects was similar between the two groups. Patients with abnormal BPR had the higher prevalence of LVCD as compared to those with normal BPR (47.1 vs. 10%, p < 0.0002). Multiple logistic regression analysis revealed that LVCD was independently associated with abnormal BPR (odds ratio 3.76, 95% confidence interval 1.61 to 8.76). CONCLUSIONS: Exercise-induced abnormal BPRs in patients with HCM are related to subendocardial ischemia during exercise.

Adolescent↗

PubMed2002

Loss of reflex inhibition following muscle tendon stimulation in essential tremor.

Electrical stimulation of human upper limb muscle tendons produces a reflex inhibition (I(1)) in the same muscles. This inhibition is reduced in Parkinson's disease (PD), prompting a similar study of essential tremor (ET). In essential tremor, two of eight subjects had no discernible inhibition, even following supramaximal stimulation (< 80 mA) of the tendons from extensor digitorum communis and extensor pollicis brevis. In the remaining six subjects, the mean thresholds for I(1) in these muscles were increased by 270 and 320%, respectively, relative to controls. The maximal amplitude of the inhibition was significantly reduced in the ET group, as was the following excitation (E(1)). The latency and duration of I(1) were not different in ET subjects and controls. The maximal duration of I(1) was correlated with tremor frequency in individuals, and tendon stimulation was effective in initiating ongoing tremor cycles. These results disclose a peripheral reflex abnormality in ET that is mediated by tendon afferents and can be linked to the coexistent tremor. The response in ET was distinguished from that in PD by its different time-course and by failure of the response to appear in the antagonist muscle. The abnormality may prove a useful marker for ET, which currently lacks a definitive pathological or neurophysiological marker to support objective clinical diagnosis.

Electric Stimulation↗

PubMed1995

Neurological complications of acquired cobalamin deficiency: clinical aspects.

Neuropsychiatric syndromes occur in about 40% of Cbl-deficient patients and are characterized by progressive and variable damage to the spinal cord, peripheral nerves and cerebrum. The first abnormality is usually sensory impairment, most often presenting as distal and symmetrical paraesthesiae of the lower limbs and frequently associated with ataxia. Almost all patients demonstrate loss of vibratory sensation, often in association with diminished proprioception and cutaneous sensation and a Romberg sign. Corticospinal tract involvement is common in more advanced cases, with abnormal reflexes, motor impairment and, ultimately, spastic paraparesis. A minority of patients exhibit mental or psychiatric disturbances or autonomic signs, but these rarely if ever occur in the absence of other neurological changes. Because N2O inactivates Cbl, abuse of the gas may lead to typical Cbl neuropathy. Haematological changes are minimal and serum Cbl levels and Schilling tests normal in most patients. The severity of neurological abnormalities prior to treatment correlates with the duration of symptoms and the haemoglobin level. Initial severity, symptom duration and initial haemoglobin also correlate with residual neurological damage after Cbl therapy. The inverse correlation between severity of anaemia and neurological damage is not understood. Diagnosis of Cbl neuropathy can usually be made in the presence of the typical neuropsychiatric abnormalities, a low serum Cbl level and evidence of megaloblastic haemopoiesis. In some patients serum MMA and HCYS determinations or a therapeutic trial may be required. A neurological response usually occurs within the first 3 months, although further improvement may occur with time. Patients with advanced disease may be left with major residual disability. Therefore early diagnosis is critical. Pharmacological doses of folic acid reverse the haematological abnormalities of Cbl deficiency. This may allow neuropathy to develop or progress and make recognition of deficiency more difficult. There is no clear evidence that folic acid therapy precipitates or exacerbates Cbl neuropathy. Haematological improvement may occur in a fraction of patients receiving small doses of folate, but the data are inadequate to predict the danger of low levels of folate supplementation in the general population.

Humans↗

PubMedDate not supplied

Vestibular system abnormalities in otosclerotic subjects.

A technique to quantify the tandem Romberg test (posturography) was used to study ten patients with otosclerosis before (series 1), 48 hours after (series 2), and between two to four months after (series 3) a stapedectomy. The results were analyzed by power spectrum analysis and then compared to findings from electronystagmographic testing performed with series 1 and 3. There was no significant change in the electronystagmography (ENG) test findings between series 1 and 3. Posturography, however, demonstrated an uncompensated vestibular pattern in the immediate postoperative period which, after two months, converted to a compensated vestibular pattern. Posturography serves as a useful quantitative test for the study of patients with balance disorders because the procedure supplements rather than complements the ENG. In addition, posturography detects vestibular reflex abnormalities in stapedectomized patients two months afterwards. Other testing modalities have not consistently demonstrated this postoperative vestibular system instability.

Adult↗