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At least 469 records · Page 26Linked to original sources
PubMed1999

Hyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-GM1 antibody.

OBJECTIVES: To investigate the incidence of hyperreflexia in patients with Guillain-Barré syndrome (GBS), and its relation with electrodiagnosis of acute motor axonal neuropathy (AMAN), antiganglioside GM1 antibody, and Campylobacter jejuni infection. It was reported that patients with AMAN in northern China often had hyperreflexia in the recovery phase. METHODS: In 54 consecutive Japanese patients with GBS, sequential findings of tendon reflexes were reviewed. By electrodiagnostic criteria, patients were classified as having AMAN or acute inflammatory demyelinating polyneuropathy (AIDP). Anti-GM1 and anti-C jejuni antibodies were measured by enzyme linked immunosorbent assays. RESULTS: Seven (13%) patients developed hyperreflexia with the spread of the myotatic reflex to other segments in the early recovery phase, one of whom already had hyperreflexia in the acute progressive phase. Of the seven patients, six had AMAN and all seven had anti-GM1 antibodies, whereas only two had anti-C jejuni antibodies. Hyperreflexia was more often found in patients with AMAN than AIDP (6/23 v 1/18, p=0. 002), and in patients with anti-GM1 antibodies than without them (7/26 v 0/28, p=0.01). Hyperreflexic patients had milder peak disabilities than patients without hyperreflexia (p=0.03). Increased motor neuron excitability in the hyperreflexic patients was supported by increased soleus H-reflex amplitudes and the appearance of H-reflexes in the small hand or foot muscles. CONCLUSIONS: Hyperreflexia often occurs in patients with GBS especially with AMAN, anti-GM1 antibodies, and milder disease. Increased motor neuron excitability further characterises the subgroup of patients with GBS with AMAN and anti-GM1 antibodies.

Acute Disease↗
PubMed2002

Six novel connexin32 (GJB1) mutations in X-linked Charcot-Marie-Tooth disease.

X-linked Charcot-Marie-Tooth disease (CMTX) is a clinically heterogeneous hereditary motor and sensory neuropathy with X-linked transmission. Common clinical manifestations of CMTX, as in other forms of Charcot-Marie-Tooth disease (CMT), are distal muscle wasting and weakness, hyporeflexia, distal sensory disturbance, and foot deformities. Motor nerve conduction velocity is reduced. In male patients it is often less than 38 m/s in the median nerve (a value often used to distinguish between "demyelinating" and "axonal" forms of CMT), but in female patients conduction velocity may be faster than this or normal. Mutations in the connexin32 (gap junction protein beta 1 (GJB1)) gene are responsible for the majority of CMTX cases. This report describes six British CMTX families with six novel mutations (four missense, one nonsense, and one frame shift) of the GJB1 gene. Affected members in these six families had typical signs of CMT but in some affected members of three families there was additional central nervous system involvement or deafness in the absence of any other explanation other than CMT.

Adolescent↗
PubMed2004

Effect of thermal stress on the vestibulosympathetic reflexes in humans.

Both heat stress and vestibular activation alter autonomic responses; however, the interaction of these two sympathetic activators is unknown. To determine the effect of heat stress on the vestibulosympathetic reflex, eight subjects performed static head-down rotation (HDR) during normothermia and whole body heating. Muscle sympathetic nerve activity (MSNA; peroneal microneurography), mean arterial blood pressure (MAP), heart rate (HR), and internal temperature were measured during the experimental trials. HDR during normothermia caused a significant increase in MSNA (Delta5 +/- 1 bursts/min; Delta53 +/- 14 arbitrary units/min), whereas no change was observed in MAP, HR, or internal temperature. Whole body heating significantly increased internal temperature (Delta0.9 +/- 0.1 degrees C), MSNA (Delta10 +/- 3 bursts/min; Delta152 +/- 44 arbitrary units/min), and HR (Delta25 +/- 6 beats/min), but it did not alter MAP. HDR during whole body heating increased MSNA (Delta16 +/- 4 bursts/min; Delta233 +/- 90 arbitrary units/min from normothermic baseline), which was not significantly different from the algebraic sum of HDR during normothermia and whole body heating (Delta15 +/- 4 bursts/min; Delta205 +/- 55 arbitrary units/min). These data suggest that heat stress does not modify the vestibulosympathetic reflex and that both the vestibulosympathetic and thermal reflexes are robust, independent sympathetic nervous system activators.

Adult↗
PubMed2003

Phenytoin protects spinal cord axons and preserves axonal conduction and neurological function in a model of neuroinflammation in vivo.

Axonal degeneration within the spinal cord contributes substantially to neurological disability in multiple sclerosis (MS). Thus neuroprotective therapies that preserve axons, so that they maintain their integrity and continue to function, might be expected to result in improved neurological outcome. Sodium channels are known to provide a route for sodium influx that can drive calcium influx, via reverse operation of the Na+/Ca2+ exchanger, after injury to axons within the CNS, and sodium channel blockers have been shown to protect CNS axons from degeneration after experimental anoxic, traumatic, and nitric oxide (NO)-induced injury. In this study, we asked whether phenytoin, which is known to block sodium channels, can protect spinal cord axons from degeneration in mice with experimental allergic encephalomyelitis (EAE), which display substantial axonal degeneration and clinical paralysis. We demonstrate that the loss of dorsal corticospinal tract (63%) and dorsal column (cuneate fasciculus; 43%) axons in EAE is significantly ameliorated (corticospinal tract: 28%; cuneate fasciculus: 17%) by treatment with phenytoin. Spinal cord compound action potentials (CAP) were significantly attenuated in untreated EAE, whereas spinal cords from phenytoin-treated EAE had robust CAPs, similar to those from phenytoin-treated control mice. Clinical scores in phenytoin-treated EAE at 28 days were significantly improved (1.5, i.e., minor righting reflex abnormalities) compared with untreated EAE (3.8, i.e., near-complete hindlimb paralysis). Our results demonstrate that phenytoin has a protective effect in vivo on spinal cord axons, preventing their degeneration, maintaining their ability to conduct action potentials, and improving clinical status in a model of neuroinflammation.

Animals↗
PubMed2006

Changes in stretch reflex excitability are related to "giving way" symptoms in patients with anterior cruciate ligament rupture.

A rupture of the anterior cruciate ligament (ACL) usually leads to an altered stretch reflex excitability of the thigh muscles that stabilize the knee. The purpose of this study was to quantitatively assess reflex activity in the m. semitendinosus/semimembranosus after anterior tibial translation in 21 patients with isolated ACL ruptures. The patients were divided into a group with "giving way" symptoms (noncopers, n = 12) and a group without "giving way" symptoms (copers, n = 9). While the patients were standing upright with 30 degrees knee flexion, a force of 300 N was applied to the knee to induce posterior-anterior tibial translation. Activity of m. semitendinosus/semimembranosus was measured using surface electromyography (EMG). A linear potentiometer was placed on the tibial tuberosity and measured maximum tibial translation during standing (i.e., functional condition). In addition, knee laxity was assessed with a KT1000 arthrometer under passive conditions. After ACL rupture, the short-latency response (SLR) latency remained unchanged (P = 0.21), whereas for the medium-latency response (MLR) it was significantly longer (P < 0.001). Significantly longer MLR latencies were noted for noncopers compared with copers (P < 0.01), whereas SLR latencies were similar. Significant differences between healthy and injured legs were noted after tibial translations using KT1000 (P < 0.001) and during stance (P < 0.001). Mechanical knee instability was found to be unchanged between copers and noncopers (KT1000: P = 0.97; tibial translation: P = 0.31). These results indicate that ACL rupture is associated with altered stretch reflex excitability, which may lead to "giving way" symptoms, and that altered stretch reflex excitability may be more important for the development of "giving way" than the mechanical instability of the knee.

Adult↗
PubMed1976

Inhibition of feline collateral vessel development following experimental thrombolic occlusion.

We compared development of feline hindlimb collateral circulation after acute occlusion of the terminal aorta by ligation, thrombus formation, and formation of a "closed" aortic loop containing thromboplastin. Collateral circulation development was assessed by aortograms, scintillation scans, neurological signs following occlusion, measurement of hindlimb muscle blood flow, and forelimb and hindlimb temperature. In cats in which aortic occlusion was the result of ligation or thromboplastin in the aortic loop, paralysis was not evident. Aortograms and scintillation scans indicated hindlimb blood flow. Both muscle temperature and blood flow data indicated that the return of blood flow was rapid. The 5th lumbar artery appears to be the origin of the collateral vessels. The mid-zone component is a dorsal and ventral vertebral route and an epaxial muscle route. The reentry components are the 6th or 7th lumbar arteries. The collateral vessels arise from preexisting collateral vessels. Of those cats in which aortic occlusion was the result of a thrombus, all exhibited paralysis. Aortograms, scintillation scans, muscle temperature, and hindlimb blood flow data indicated reduced hindlimb blood flow. The results suggest that the thrombus has an inhibitory effect on the development of collateral circulation.

Acute Disease↗
PubMed1995

Asymmetrical skin temperature in ischemic stroke.

BACKGROUND AND PURPOSE: Sympathetic dysfunction is known to manifest commonly in stroke as cardiovascular and sudomotor dysregulation, but the knowledge so far obtained concerning skin temperature and vasomotor changes in cerebrovascular diseases is contradictory. The purpose of the present study was to evaluate cutaneous temperature in ischemic stroke in a prospective follow-up study. METHODS: Skin temperature was measured at five sites on each side of the body at rest and after a heating stimulus in 44 patients with a hemispheric infarction, and in 19 patients with a brain stem infarction, in the acute phase and at 1 month and at 6 months after the infarction. RESULTS: Skin temperatures on the forearm, leg, and foot on the side contralateral to the site of infarction were significantly lower than on the ipsilateral side during the whole 6-month follow-up period. Asymmetrical temperature was associated with the presence of pyramidal tract signs in hemispheric infarction and with the presence of Wallenberg's syndrome in brain stem infarction. In hemispheric infarction, the degree of asymmetrical temperature correlated with the severity of limb paresis. CONCLUSIONS: A temperature decline in the limbs contralateral to the site of infarction seems to be a frequent, long-lasting consequence of autonomic failure in patients with stroke. The phenomenon seems to be associated with pyramidal tract signs and the presence of Wallenberg's syndrome.

Acute Disease↗
PubMed2003

Usher syndrome type III can mimic other types of Usher syndrome.

Clinical and genetic characteristics are presented of 2 patients from a Dutch Usher syndrome type III family who have a new homozygous USH3 gene mutation: 149-152delCAGG + insTGTCCAAT. One individual (IV:1) is profoundly hearing impaired and has normal vestibular function and retinitis punctata albescens (RPA). The other individual is also profoundly hearing impaired, but has well-developed speech, vestibular areflexia, and retinitis pigmentosa sine pigmento (RPSP). These findings suggest that Usher syndrome type III can be clinically misdiagnosed as either Usher type I or II; that Usher syndrome patients who are profoundly hearing impaired and have normal vestibular function should be tested for USH3 mutations; and that RPA and RPSP can occur as fundoscopic manifestations of pigmentary retinopathy in Usher syndrome.

Adult↗
PubMed1994

Does intracochlear implantation jeopardize vestibular function?

We present the results of the vestibular function tests of 35 patients who were selected for cochlear implantation. Vestibular function was evaluated with a caloric test and a velocity step test. The preimplant data were compared to those in previously reported series. Intracochlear implantation was performed in 25 patients. The vestibular complications encountered in this group are presented and discussed. Six patients had normal or residual (but substantial) vestibular function in the ear eligible for implantation. Vestibular function was preserved in 3 patients and was lost in 3 patients, in 1 case through an iatrogenic cause. We estimate the risk of losing vestibular function as a result of intracochlear implantation as between 50% and 60% on the basis of the present and previously reported data.

Adult↗
PubMed1987

The neurological assault on the great toe (1893-1911).

The late 19th/early 20th century heralded a period in neurology when there was claim and counter claim about the founders of new reflex movements of the great toe. The cutaneous plantar reflex is undoubtedly one of the most important signs in clinical neurology, and there have been several methods described of eliciting this sign, each with its own eponymous name. This article reviews the background to these claims and the contribution of the various authors, to the discovery, clinical relevance and ease of eliciting reflex movements of the great toe.

Germany↗
PubMed2004

Familial hyperekplexia and refractory status epilepticus: a new autosomal recessive syndrome.

Hyperekplexia is a rare disorder characterized by an exaggerated startle response to noise and handling and by neonatal hypertonia. It is predominantly an autosomal dominant disease; however, atypical cases with additional variable manifestations have been reported. We report a hitherto undescribed association of hyperekplexia and refractory status epilepticus in two siblings. Both children were born after an uneventful pregnancy to healthy unrelated Ashkenazi Jews. Both had increased startle and tone from birth and later became hypotonic. A metabolic evaluation, including a muscle biopsy, was normal. At the age of 18 months and 12 months, respectively, they developed status epilepticus refractory to all treatment that culminated in death. An autopsy in the girl did not reveal any brain pathology. The unusual association of hyperekplexia and refractory status epilepticus in both children suggests that this is a new autosomal recessive syndrome, possibly a channelopathy affecting both the brain and the spinal cord.

Female↗
PubMed1986

Reflex epilepsy.

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Acoustic Stimulation↗
PubMed1998

"Extensor toe sign" by various methods in spastic children with cerebral palsy.

Upper motor neuron lesion in adults is usually associated with spasticity and "extensor toe sign" on plantar stimulation (extensor plantar response). There are various methods of eliciting this sign including the classic method by Babinski. Other methods produce this response when the area of reflexogenic zone is increased due to upper motor neuron lesion. There are varying reports of Babinski positivity in spastic cerebral palsy. This study was undertaken to assess the sensitivity of different methods of eliciting "extensor toe sign." An attempt has also been made to correlate the severity of spasticity with the combined "extensor toe sign" positivity by various methods and with the increase in reflexogenic zone. Eighty-one children with spastic cerebral palsy were examined. Twelve had hemiplegia; therefore, a total of 150 limbs were tested. "Extensor toe sign" was elicited by 12 different methods in each patient. The sensitivity of each method was calculated and compared with each other one. The assessment of spasticity was done using the Ashworth Tone Scale. The severity of spasticity was correlated with "extensor toe sign" positivity using various methods. Classic Babinski reflex was positive in 75% of cases, whereas Gonda-Allen sign was positive in 90% of cases followed by Allen-Cleckley (82%), Chaddock (74%), and Cornell (54%). All other signs had sensitivity of less than 30%. There was no increase in sensitivity after combining them. There was significant negative correlation between the spasticity and the combined "extensor toe sign" positivity (by all the methods). This study, therefore, suggests that the majority of patients with spastic cerebral palsy have positive "extensor toe sign." The Gonda-Allen method is more sensitive than the classic Babinski method. A positive "extensor toe sign" is negatively correlated to the degree of spasticity.

Adolescent↗
PubMedDate not supplied

Deep tendon reflexes: the what, why, where, and how of tapping.

Deep tendon reflexes demonstrate the homeostasis between the cerebral cortex and the spinal cord. When these reflexes are disrupted, hyperreflexia (disease induced) or hyporeflexia/areflexia (drug induced) occurs. Although nurses perform deep tendon reflex assessments regularly, it is difficult to incorporate theoretical principles in these assessments because of scant medical literature, a lack of nursing research, and time constraints in nursing programs. These conditions usually result in one-on-one training, causing reduced consistency. A comprehensive examination assists the clinician to apply theoretical principles, develop expert technique, and serve as a catalyst for clinical research.

Humans↗
PubMed1986

Transient cerebral dysfunction secondary to high-dose methotrexate.

A transient acute neurologic syndrome occurred in 22 patients receiving high-dose methotrexate (HDMTX) (8 to 9 g/m2) for a variety of malignancies. The neurologic signs were similar in all cases. The syndrome occurred an average of six days after the second or third weekly treatment. Common findings included behavioral abnormalities, focal sensorimotor signs, and abnormal reflexes. Signs often alternated from one side to the other. Evaluations including computed tomography (CT) scan, lumbar puncture, hemogram, and blood chemistry were normal. The EEG revealed some slowing in all cases. The cause of this syndrome is unknown. It is transient and usually does not recur. Its appearance does not preclude further treatment with HDMTX.

Adolescent↗