Hoffmann reflex abnormalities in psychotic patients.
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PURPOSE: The aim of the present study was to evaluate the efficacy of blink reflex as a method for obtaining early diagnosis of cranial nerve involvement in alcoholic patients. MATERIALS AND METHODS: The study was conducted on 30 male alcoholics with a mean age of 43 years. They had histories of alcohol abuse for at least 6 years (mean: 25). At the time of recording, they had undergone detoxification treatment for a mean of 27 days. RESULTS: R1 (early response), R2Y (second ipsilateral response), and R2C (second contralateral response) latencies in alcoholics were prolonged relative to controls and the differences were statistically significant (p < 0.02, p < 0.001, p < 0.001, respectively). According to the defined criteria, 40% of the patients had abnormal responses, and the most common abnormality was the unilateral prolongation of R1 (13%). CONCLUSION: Finding abnormal blink reflex responses in alcoholic patients has suggested that blink reflex testing is a useful method for the evaluation of subclinical cranial nerve involvement in alcoholic patients. Blink reflex testing may be useful in detecting early changes and in the follow-up of alcoholic disorder.
Congestive heart failure (CHF) is characterized by a sympathetic activation and a baroreflex impairment whose degree is directly related to the clinical severity of the disease. However, whether these abnormalities vary according to the ischaemic or idiopathic dilated nature of the CHF state has not been conclusively documented. In patients with a clinically stable, chronic CHF state in New York Heart Association functional class II and III, due either to ischaemic heart disease (IHD; n=22, age 60.3+/-2.4 years, means+/-S.E.M.) or to idiopathic dilated cardiomyopathy (IDC; n=20, age 58.9+/-2.8 years), and in 30 age-matched controls, we measured arterial blood pressure (using a Finapres device), heart rate (by electrocardiogram) and postganglionic muscle sympathetic nerve traffic (by microneurography) at rest and during baroreceptor manipulation induced by the vasoactive drug-infusion technique. Blood pressure values were not significantly different in CHF patients and controls. Compared with controls, heart rate was similarly increased and left ventricular ejection fraction (by echocardiography) similarly reduced in CHF patients with IHD or IDC. Muscle sympathetic nerve traffic was significantly greater in CHF patients than in controls, and did not differ between patients with IHD or IDC (67.3+/-4.2 and 67.8+/-3.8 bursts/100 heart beats respectively). This was also the case for the degree of baroreflex impairment. These data show that CHF states due to IHD or to IDC are characterized by a similar degree of peripheral sympathetic activation and by a similar impairment of the baroreflex function. Thus the neuroadrenergic and reflex abnormalities characterizing CHF are independent of its aetiology.
OBJECTIVE: The aim was to investigate the effect of cardiac transplantation on reflex control of lower leg subcutaneous blood flow. METHODS: The reflex regulation of subcutaneous blood flow of the lower leg was studied in 11 patients following orthotopic cardiac transplantation, in 11 patients with severe congestive heart failure (New York Heart Association functional class III or IV), and in 11 healthy subjects. Four patients were studied before and after cardiac transplantation. Cause of heart failure was classified as idiopathic dilated cardiomyopathy in all heart failure patients and in all the cardiac transplant patients before transplantation. Blood flow was measured by the local 133xenon washout method in the supine position and during 45 degrees head up tilt. RESULTS: When performing head up tilt without activation of the local nervous venoarteriolar axon reflex in patients with congestive heart failure, the relative subcutaneous blood flow increased abnormally, by 50(SD 25)%, but in patients after cardiac transplantation a normal decrease was seen [-28(13)%, p < 0.001]. The responses in the transplant group were similar to those observed in normal controls with a decrease in blood flow [-32(15)%; NS]. Head up tilt with simultaneous activation of the local venoarteriolar axon reflex increased blood flow [31(22)%] in patients with heart failure as compared to the decrease in blood flow found in the transplants [-44(17)%, p < 0.001]. The decrease of blood flow was not significantly different between the transplant group and control subjects [-53(19)%; NS]. CONCLUSIONS: These results indicate that abnormal reflex regulation in severe congestive heart failure with peripheral vasodilation of the lower leg during orthostasis is reversed and even normalised after cardiac transplantation. The haemodynamic consequence may be a regaining of an oedema-protective mechanism that eliminates the stress (capillary hypertension) on the microcirculation seen in severe heart failure.
H-reflex was studied in 43 patients with low back pain (including 20 patients with neurological deficit corresponding to S1 radix and 23 patients without deficit) and 20 control subjects. Among patients with neurological deficit the abnormality consisted of absent H-reflex (7 patients), increased H-latency (3 patients), reduced H/M maximal amplitude ratio (5 patients) or a combination of the latter two (2 patients). The H/M ratio was significantly reduced in this group as compared to control subjects and between affected and unaffected sides. Abnormal H-reflex correlated well with ankle jerk hypo- or areflexia, S1 sensory deficit and lumbar myelographic/CT abnormality. In 23 patients without deficit, increased H-latency and/or reduced H/M ratio was observed in 4 cases. Enhanced H/M ratio was noted in only 2 patients of this group. Use of H/M ratio seems to increase the sensitivity of H-reflex in the diagnosis of S1 radiculopathy.
We investigated the brainstem blink reflex in patients suffering from idiopathic and symptomatic trigeminal neuralgia to establish possible dysfunction in the reflex cycle and determine eventual differences between the two disease types. The study included 35 patients with idiopathic disease and seven patients with symptomatic disease, their results compared with those of 50 normal controls. We stimulated the forehead afferents of the supraorbital nerve and recorded the response from both orbicularis oculi muscles. We tested latencies of bilateral late components (R2, R2'), irritative R3 component and the incidence of R3 component. The patients with idiopathic trigeminal neuralgia showed normal parameters of blink reflex, except for the greater incidence of R3 component. Patients with symptomatic trigeminal neuralgia showed prolonged latencies of R2, R2' and R3 components when stimulating the afflicted side, but no significant difference in incidence of R3 component compared with the control group. The results indicate that abnormalities of blink reflex are significantly different in the two groups of patients. The high incidence of R3 component seems to be typical of idiopathic disease, whereas the prolonged latencies of late reflex components after stimulation of the afflicted side seem to be typical for symptomatic disease. These results suggest that testing the blink reflex may prove a significant aid in distinguishing the idiopathic and symptomatic disease types.
OBJECTIVE: To investigate the high-frequency vestibulo-ocular reflex (VOR) in patients with migraine, with and without dizziness and aura. BACKGROUND: Migraine is a common cause of dizziness. Although many vestibular testing abnormalities have been documented in migraine patients, high-frequency VOR abnormalities have not been reported. METHODS: Thirty-nine consecutive patients with migraine were studied with the vestibular autorotation test (VAT). The patients were subclassified as having migraine headache only, migraine with visual aura, migraine with dizziness, or migraine with visual aura and dizziness. RESULTS: Only a high vertical phase in the 4 to 5 Hz range was correlated with migraine (correlation coefficients: .356, P=.03). Further analysis revealed that an abnormal 4 to 5 Hz vertical phase result also was positively correlated with migraine with aura and dizziness (correlation coefficients: .392). CONCLUSION: The results suggest that patients with migraine may have an abnormal vertical VOR at higher head movement frequencies. Migraine patients with visual aura and dizziness are even more likely to have this abnormality.
Previous anatomic and physiologic studies suggest brainstem dysfunction in cranial-cervical dystonia. To further explore this, we studied suprathreshold acoustic reflex waveforms in 15 such patients. A unique feature of this technique is its ability to reject movement artifacts before averaging the acoustic reflex waveforms. Thirteen patients (87%) showed some abnormality in reflex waveform morphology. There were both amplitude and latency abnormalities. These findings support the hypothesis that cranial-cervical dystonia reflects dysfunction of the brainstem.
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BACKGROUND: Damage of the peripheral nervous system is particularly frequent in diabetes mellitus (DM), but somatic cranial neuropathies usually presenting as mononeuropathies are rare. Oculomotor and facial nerves are among the most commonly affected, whereas the Vth, IXth and Xth cranial nerves are less often affected. While existing neurophysiological tests in the subclinical diagnosis of damage to the peripheral nerve in diabetic patients have advanced, the same does not hold true for the subclinical diagnosis of the central nervous system (CNS). Electrophysiological studies such as the blink reflex was shown to be an effective method for revealing subclinical involvement of cranial nerves in generalised neuropathies. The aim of the present study was to evaluate the efficacy of blink reflex as a method for obtaining early diagnosis of cranial nerve involvement in diabetic patients frequently affected with peripheral neuropathy. METHODS: Twenty diabetic patients with electrophysiologically confirmed neuropathy were included in the present study for the evaluation of blink reflex. Patients with earlier cranial nerve involvement were excluded. RESULTS: Abnormal blink reflex responses were found in 55% of patients studied. R2Y and R2C latencies in diabetic patients were prolonged relative to controls (p<0.001 and p<0.001, respectively). However R1 values in diabetic patients did not differ significantly from those of normal controls (p<0.5). R2Y and R2C prolongation showed a positive correlation with the duration of disease (p=0.015 and p=0.009, respectively). However the same correlation could not be found with R1 values. No correlations were found between R1, R2Y, R2C values and HbA(1c) nor between R1, R2Y, R2C values and patients' age. CONCLUSION: We suggest that blink reflex testing is a useful method for obtaining early diagnosis of cranial nerve compromise in diabetic patients who do not show any clinical symptoms or signs of CNS involvement.
Thirteen patients suffering from multiple sclerosis were analyzed by a Madsen ZO 70 electroacoustic bridge connected to an electronystagmograph through an impedance adaptor. Threshold, amplitude, decay and difference limen of intensity (DLI) of the stapedius reflex were examined for the frequencies 500, 1 000, 2 000 and 4 000 Hz. The difference between standard audiometric results and stapedius reflex data stresses the value of reflex measurements in assessing brain stem pathology.
Visual modulation of the vestibulo-ocular reflex (VOR) was analyzed in 16 patients with non-neurologic Behçet's disease who had no manifest vestibular or ocular-motor symptoms. The VOR gains in the darkness were elevated in 63% of the patients. The elevated gain in the darkness was not attributed with certainty to vestibular adaptation to defective smooth pursuit, because only 25% of the patients manifested impaired smooth pursuit eye movements. Visual impairment occurred in some patients but did not correlate with the VOR elevation. An unknown mechanism affecting the vestibular system has been considered. The VOR elevation in the darkness may suggest the presence of a latent brainstem abnormality in the patients.
As electrical stimulation of the rectum has been shown to result in reflex internal sphincter inhibition mediated by intrinsic nerves, we aimed to evaluate the integrity of these nerves in the rectum of diabetic patients. Anal canal pressure, recto-anal inhibitory reflex (RAIR) and continence were evaluated in 30 diabetic patients (male:female 13:17, median age 57 years, range 37-70) and these data were compared with similar data obtained from 22 age- and sex-matched healthy controls (male:female 9:13, median age 51 years, range 19-65 years). Median duration of diabetes was 8 years (range 3-30). Twelve (40%) of the 30 diabetics had impaired continence for gas (n = 12) and liquid faeces (n = 3). None of the controls had incontinence. Median maximum resting anal canal pressure (MRP) was: patients 30 mmHg (range 20-75 mmHg) versus controls 40 mmHg (range 20-105 mmHg, P = 0.61). Median maximum squeeze pressure (MSP) was 65 mmHg (range 30-150 mmHg) in patients versus 84mmHg (range 35-230 mm Hg) in controls (P = 0.59). Median threshold rectal mucosal electrosensation (RMES-T) was 27mA (5-40 mA) in patients versus 13 mA (5-28 mA) in controls (P = 0.03). Maximum tolerable rectal mucosal electrosensation was 40 mA (20-60) in patients versus 20 mA (10-30), in controls (P = 0.042, all comparisons using the Wilcoxon rank test). Recto-anal inhibitory reflex was present in eight, abnormal in five (one incontinent) and absent in 17 (11 incontinent) diabetics, while it was present in 18 and abnormal in four controls (test of proportion, P = 0.031). Blood glucose in diabetics on the day of the procedure was 98 mg/dL (70-165 mg/dL). Rectal mucosal electrosensitivity and RAIR were impaired in significantly more patients with diabetes than controls, implying impairment of intrinsic neuronal function. The recto-anal inhibitory reflex was either impaired or absent in all diabetic patients with incontinence.
AIMS/HYPOTHESIS: Previous studies have shown that alterations in vascular, metabolic, inflammatory and haemocoagulative functions characterise the metabolic syndrome. Whether this is also the case for sympathetic function is not clear. We therefore aimed to clarify this issue and to determine whether metabolic or reflex mechanisms might be responsible for the possible adrenergic dysfunction. METHODS: In 43 healthy control subjects (age 48.2+/-1.0 years, mean+/-SEM) and in 48 untreated age-matched subjects with metabolic syndrome (National Cholesterol Education Program's Adult Treatment Panel III Report criteria) we measured, along with anthropometric and metabolic variables, blood pressure (Finapres), heart rate (ECG) and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor manipulation (vasoactive drug infusion technique). RESULTS: Compared with control subjects, subjects with metabolic syndrome had higher BMI, waist circumference, blood pressure, cholesterol, triglycerides, insulin and homeostasis model assessment (HOMA) index values but lower HDL cholesterol values. Sympathetic nerve traffic was significantly greater in subjects with metabolic syndrome than in control subjects (61.1+/-2.6 vs 43.8+/-2.8 bursts/100 heartbeats, p<0.01), the presence of sympathetic activation also being detectable when the metabolic syndrome did not include hypertension as a component. Muscle sympathetic nerve traffic correlated directly and significantly with waist circumference (r=0.46, p<0.001) and HOMA index (r=0.49, p<0.001) and was inversely related to baroreflex sensitivity (r=-0.44, p<0.001), which was impaired in the metabolic syndrome. CONCLUSIONS/INTERPRETATION: These data provide evidence that the metabolic syndrome is characterised by sympathetic activation and that this abnormality (1) is also detectable when blood pressure is normal and (2) depends on insulin resistance as well as on reflex alterations.
OBJECTIVES: We sought to compare the forearm reflex venous response to mental arithmetic stress in patients with neuromediated syncope and in normal subjects. BACKGROUND: Patients with neuromediated syncope have a paradoxic arterial vasodilation in response to stressors that usually provoke vasoconstriction. Given the postulated role of diminished preload in provoking the reflex responses resulting in syncope, we hypothesized that mental stress might provoke paradoxic reflex venodilation in patients with neuromediated syncope. METHODS: Twelve normal subjects (mean age [+/-SD] 47 +/- 9 years) and 27 patients with neuromediated syncope (mean age 42 +/- 13 years) were studied before and during a mental arithmetic stress test. Forearm venous pressure-volume relations were determined by using radionuclide plethysmography. RESULTS: During mental arithmetic stress, heart rate and systolic and diastolic blood pressure increased significantly and similarly both in normal subjects and in patients with neuromediated syncope. The heart rate and blood pressure changes were qualitatively similar in both groups. However, with mental arithmetic stress, forearm venoconstriction of 13 +/- 2% (mean +/- SEM) was noted in normal subjects (p < 0.001) but not in patients with neuromediated syncope (mean 2%, p = NS). This group response of patients with neuromediated syncope did not result from a lack of individual responses but occurred because these patients had a wide range of responses. The normal physiologic and methodologic variability of the method was +/- 4%. Thirteen of the 27 patients with neuromediated syncope had forearm venoconstriction of 14.5 +/- 6.8% during mental arithmetic stress, whereas 7 had paradoxic forearm venodilation of 14.6 +/- 8.8%, and 7 were considered nonresponders (-1.3 +/- 3.4%). Thus, 14 (52%) of the 27 patients with syncope did not have normal vasoconstriction in response to mental stress. CONCLUSIONS: Patients with neuromediated syncope have an abnormal range of forearm venomotor responses to mental arithmetic stress. Reflex control of the veins may play an important role in the pathogenesis of neuromediated syncope.
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The eye movements of 15 patients with Vogt-Koyanagi-Harada (VKH) syndrome were analysed. Transient dizziness occurred in 60% of the patients. Eight patients (53%) exhibited horizontal jerk nystagmus that was completely inhibited by visual fixation. Eight cases (53%) exhibited the elevation of vestibulo-ocular reflex (VOR) gain in darkness. Six of the patients with nystagmus had defective smooth pursuit movements with reduced gain on the side ipsilateral to the nystagmus. Saccadic and optokinetic eye movements were intact, and visual vestibular interaction was also normal. Impaired eye movements in VKH syndrome may be caused by asymmetry of the vestibular function secondary to the labyrinthine inflammation.
Systemic administration of the mitochondrial toxin 3-nitropropionic acid (3NP) to rats produces striatal lesions that mimic some aspects of pathology in Huntington's disease (HD). To evaluate whether 3NP-induced lesions cause sensorimotor gating deficits observed in HD, we measured prepulse inhibition (PPI) of the acoustic startle reflex after systemic administration of 3NP (10, 15, or 20 mg/kg) to 5-month-old rats. PPI, the reduction of startle magnitude by a weak auditory prestimulus, is significantly reduced in patients with HD. Two daily injections of 3NP produced gross histologic evidence of striatal lesions in some rats and significantly reduced PPI. Striatal lesions also significantly disrupted amphetamine-induced stereotypy, another index of dorsal striatal function. 3NP thus reproduces a specific objective and quantifiable gating deficit found in patients with HD.