Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “REFLEX, TENDON”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed2000

Mild axonal neuropathy of children during treatment for acute lymphoblastic leukaemia.

Neurophysiological functioning was studied prospectively in children treated for acute lymphoblastic leukaemia with a low dose vincristine regime (8 x 1.5 mg/m2/dose), to obtain more insight into vincristine neuropathy. A WHO neurotoxicity score was estimated and vibration sense and electrophysiological measurements were taken at standardized times during vincristine treatment. The WHO neurotoxicity score showed decreased or disappearance of Achilles tendon reflexes, and mild sensory disturbances, but a grade 3-4 neurotoxicity was not demonstrated by any of the children. Vibration perception thresholds increased progressively during treatment and amplitudes of action potentials of peroneal and sensory ulnar and median nerves decreased, whereas nerve conduction velocities stayed unchanged. Both vibration perception thresholds and the electrophysiological findings hardly exceeded the limits of normality. We conclude that children treated for acute lymphoblastic leukaemia with a low dose vincristine regimen have mild axonal neuropathy which may be responsible for the motor problems in these children.

Achilles Tendon↗
PubMed1995

EMG before and after cervical anterior discectomy.

INTRODUCTION: In patients with cervical root syndromes, the relation between clinical findings and EMG results, the value of the registration of the H-reflex latency of the flexor carpi radial muscle (HFCR) and the rate of recovery of EMG abnormalities following surgery are unclear. METHODS: In 68 patients with cervical radicular syndromes caused by intervertebral disc lesions, EMG was made shortly before anterior cervical discectomy and four months later. EMG consisted of needle myography and bilateral determination of the HFCR. RESULTS: Results of HFCR were unrelated to findings on needle myography. Preoperative EMG abnormalities were related to more severe clinical and myelographic findings. A preoperative abnormal HFCR correlated with good clinical outcome. No relation was found between the clinical outcome and EMG-findings during follow-up. CONCLUSION: Determination of HFCR is a useful EMG-test, but further comparison to tendon reflexes is necessary. EMG identifies patients with more severe root lesions, but cannot be used for evaluation of persistent complaints within the first half year following surgery.

Cervical Vertebrae↗
PubMed1976

Spinal reflexes and the concentrations of 5-HIAA, MHPG, and HVA in lumbar cereborspinal fluid after spinal lesions in man.

Descending bulbospinal pathways that employ specific neurotransmitter substances are known to be capable of modulating segmental reflex activity in the experimental animal. To determine whether this might also occur in man correlations have been sought between the activity in spinal reflex pathways and the lumbar cerebrospinal fluid (CSF) concentrations of 5-hydroxyindolacetic acid (5-HIAA), 3 methoxy-4-hydroxyphenylglycol (MHPG), and homovanillic acid (HVA) in 12 patients with complete or virtually complete spinal lesions. The concentrations of 5-HIAA and MHPG in lumbar CSF ARE REDUCED AFTER COMPLETE OR VIRTUALLY COMPLETE SPINAL LESIONS IN MAN. This may occur within 18 days of the lesion. MHPG concentrations appear to be inversely related to the level of the lesion. The HVA concentration in lumbar CSF is reduced when there is obstruction of the CSF pathways. No relationship could be demonstrated between the concentrations of 5-HIAA or MHPG in lumbar CSF and the activity in the spinal monosynaptic pathway (estimated from the proportion of the motoneurone pool activated by the Achilles tendon reflex or H reflex) or the activity of a spinal inhibitory mechanism (estimated by the degree of vibratory inhibition of the monosynaptic reflex). Patients with a tonic vibration reflex (TVR) tended to have higher MHPG levels. There appeared to be an association between low CSF HVA and enhanced vibratory inhibition of the monosynaptic reflex in the nine patients whose spinal lesions were complete.

Adolescent↗
PubMed1989

[Electrophysiological monitoring of the brainstem function in impending brain death--serial changes of blink reflex and brainstem auditory evoked potential].

Serial changes of EEG, BR and BAEP recordings were obtained over a period of two days on two patients who had suffered massive cerebral hemorrhage while their clinical condition evolved from coma with evidence of preserved cerebral and brainstem functions to a state meeting the criteria of brain death. As clinical evidence of deteriorating brainstem function became apparent in case 1, first wave IV and V components of BAEP disappeared while waves I to III were normal. Finally, when clinical criteria of brain death were fulfilled, the BAEP response was restricted to wave I with small amplitude to stimulation of left ear only. These serial changes were likely consistent with gradual dissolution of brainstem function in a rostrocaudal direction. By contrast, in case 2, the BAEP response was restricted to waves I and II and was stationary in the whole process of impending brain death in no association with some preservation of cerebral and brainstem function. The changes of BAEP was not parallel to the progressive deterioration of EEG and BR. After meeting clinical criteria of brain death, complete abolition of waves II and I was sequential in that order, and then Babinski sign besides withdrawal and deep tendon reflexes may revive in the extremities. Monitoring of serial electrophysiological changes is helpful in the course of impending brain death to determine whether revival of Babinski sign is due to recovery of cerebral-brainstem dysfunction or due to establishment of spinal autonomy.

Aged↗
PubMed1981

[Three cases of cystic neurinoma arising from the upper cervical nerve roots and extending into the posterior cranial fossa (author's transl)].

Three cases of cystic neurinoma arising from the upper cervical spinal nerve roots and extending to the posterior cranial fossa through the foramen magnum were reported. Case 1 was a 52-year-old female presenting marked bilateral papilledema, hyperactive right knee jerk, left positive Gordon reflex and trunkal ataxia. The mass was mostly cystic and arose from the left 1st cervical nerve root. It extended to the posterior fossa, occupied the cerebello-medullary cistern and displaced the left cerebellar hemisphere posteriorly and superiorly. Case 2 was a 39-year-old male presenting marked bilateral papilledema, neck stiffness, dysfunction of the right 7, 9, 10 and 11th cranial nerves, gaze nystagmus, Horner's syndrome, right limb ataxia, and ataxic gait. The mass was totally cystic containing yellowish fluid and was growing from the right 2nd cervical spinal nerve root. The mass extended to the posterior cranial fossa up to the right cerebello-pontine angle and compressed the medulla oblongata, upper cervical cord and 7th through 11th cranial nerves on the right side. Case 3 was a 66-year-old male presenting marked bilateral papilledema, gaze nystagmus, left hemiparesis, bilateral hyperactive deep tendon reflexes, numbness of the left fingers and ataxic gait. CT scanning revealed in the midline of the posterior cranial fossa a low density mass which was enhanced in a ring-like fashion. Vertebral angiograms showed an avascular mass displacing the PICAs upwards and elongating its cranial loops antero-posteriorly. The mass was totally cystic, arose from the left 2nd cervical spinal nerve root, extended to the posterior cranial fossa and occupied the cisterna magna and vallecula. Foramen magnum syndrome was discussed and the symptoms and signs presented in these three cases were compared with those presented by foramen magnum meningioma in other reports.

Adult↗
PubMed1997

[A case of rapidly progressive HTLV-I-associated myelopathy (HAM)].

We report a 65-year-old woman with HAM who showed rapid progression of the clinical symptoms. The initial symptom was lumbago and she became unable to walk within 4 months after the onset of the lumbago. When seen on admission, she had flaccid paraplegia and areflexia was seen in the lower extremities with positive Babinski and Chaddock reflexes. She had numbness below the level of the navel, vibratory sensation was decreased in both lower limbs, and there was a hyperesthesic zone at the tenth thoracic vertebral level. She had a difficulty in urination and defecation. Laboratory examination revealed elevated anti-HTLV-I antibody titers both in serum (4,096x by PA method) and in cerebrospinal fluid (CSF) (4,096x). The levels of IgG and neopterin in CSF were also increased to 16.6 mg/dl (normal: < 5 mg/dl) and 360.3 pmol/ml (normal: < 30 pmol/ml), respectively. HTLV-I messenger RNA positive cells were detected in 0.1% to 0.01% of cells in CSF by in situ hybridization using an oligonucleotide probe labelled with alkaline phosphatase. Spinal cord MRI detected neither spinal cord compression nor vascular diseases. She was treated with 1,000 mg methylprednisolone for 3 days intravenously, followed by 60 mg oral prednisolone therapy. In several days after receiving the treatments, her muscle tonus became spastic and deep tendon reflexes in the legs became brisk. The hyperesthesia at the tenth thoracic vertebral level and numbness below the level of the navel were also gradually improved. Subsequently, her clinical features were consistant with those of the typical HAM. Therefore, the patient was diagnosed as rapidly progressive HAM. The initial phase of rapidly progressive HAM patients had been described only from clinical history. These patients had common characteristic clinical features, such as older age at onset, relatively severe motor dysfunction, high titers of anti-HTLV-I antibody in CSF, and increased levels of neopterin and IgG in CSF, when compared with those of other HAM patients. The clinical course and laboratory findings in the present patient were compatible with those in the previous cases reported as rapidly progressive HAM. This patient showed flaccid paraplegia and areflexia which have rarely been seen in HAM patients. However, these symptoms were changed to spastic and hyperactive after prednisolone therapy. We speculate that inflammation in the spinal cord in this patient was severe enough to spread to the dorsal root, and disturbed the afferent pathway from the peripheral to the central nervous system. This inflammatory reaction might be suppressed by prednisolone to facilitate the recovery of the afferent pathway, which led to the typical clinical symptoms of HAM.

Aged↗
PubMed2002

Assessment and evaluation of hereditary sensory and autonomic neuropathies with autonomic and neurophysiological examinations.

The five different types of the rare hereditary sensory and autonomic neuropathies (HSAN) are classified by their mode of inheritance, pathology, natural history, biochemical, neurophysiologic and autonomic abnormalities. Clinically, the different types of HSANs can be identified by a detailed history and examination and 'bedside' tests of sympathetic or parasympathetic function such as active standing, metronomic breathing or the Valsalva maneuver, sensory and motor nerve conduction studies, quantitative sensory testing of thermal and vibratory perception, and the analysis of sudomotor function by recordings of the sympathetic skin response (SSR) or the sweat output during quantitative sudomotor axon reflex testing (QSART). The slowly progressive, symmetrical HSAN type I manifests between the second and fourth decade with ulcers or mutilations of the lower extremities, low normal sensory and motor nerve conduction velocities, but abnormal warm, cold and heat pain perception and distal anhidrosis. In HSAN type II, symptoms occur already in infancy, trophic alterations affect fingers and toes. There are acral anhidrosis and various autonomic dysfunctions such as tonic pupils, eating and swallowing difficulties, constipation, episodic fever, profound hypotonia and episodes of apnea. Sensory perception is severely impaired and accounts for elevated vibratory but also thermal perception thresholds. Sensory nerve conduction is highly abnormal while motor nerve conduction studies are almost normal. Type III, the autosomal recessive familial dysautonomia (FD), is the most common of the HSANs. FD is characterized by pronounced autonomic, primarily sympathetic dysregulation with severe orthostatic hypotension, repeated episodes of autonomic crises with excessive arterial hypertension, profuse sweating, skin blotching, puffy hands and behavioral abnormalities. FD manifests only in children of Ashkenazi Jewish ancestry. Cardinal findings are diminished deep tendon reflexes, absence of overflow tears, absence of fungi-form papillae of the tongue and of axon flare response following intradermal histamine injection. Thermal and vibratory testing show pronounced impairment of temperature and pain but also of vibratory perception. Children with HSAN IV, 'congenital insensitivity to pain with anhidrosis' experience repeated episodes of high fevers during high environmental temperature due to anhidrosis. The anhidrosis of the hyperkeratotic skin accounts for absence of the SSR or lack of sweat output during QSART. The patients' insensitivity to superficial as well as deep, visceral pain can be demonstrated e. g. by quantitative heat pain testing. Patients develop severe mutilations e. g. of the tip of their tongue, they might have severe burn injuries and multiple, unnoticed fractures with neuropathic joints. Children with the very rare HSAN type V respond normally to tactile, vibratory or thermal stimuli, but have a selective loss of pain perception with otherwise normal neurological examination. Painful stimuli reveal no signs of discomfort.

Hereditary Sensory and Autonomic Neuropathies↗
PubMed1991

[A case of Kennedy-Alter-Sung syndrome with type IIa hyperlipidemia--study on sex hormone receptor and lipid metabolism].

A 57-year-old man of Kennedy-Alter-Sung syndrome (K-A-S) with type IIa hyperlipidemia was reported with studies of several sex hormone receptors. He noticed tremulous movements of hands on gripping at age 40 and gynecomastia at age 46. He had been pointed out to waddle since 52 years old, and also noticed difficulty in going up stairs and standing up at age 54. He was admitted to our Neurology Service on June 5, 1989. On general physical examinations, gynecomastia, eyelids xanthomas and hypertrophy of Achilles tendons were found. Neurologic examination revealed clear consciousness and slight dysarthric speech with nasal voice. Cranial nerves showed mild bilateral facial weakness, poor uvula and soft palatal movements, atrophy and weakness of bilateral sternocleidomastoid muscles, and atrophy of tongue with fasciculation. The four extremities were hypotonic, and proximal muscular atrophy and weakness of four extremities were seen. Deep tendon reflexes were absent in four extremities and fasciculation on both thighs was noted on contraction. Sensory and cerebellar functions were intact. Waddling gait and Gowers' sign were present. In K-A-S syndrome, abnormal lipid metabolism such as a family of type IIa hyperlipidemia, or familial and sporadic cases of type IV hyperlipidemia has been documented. In the family of our cases, his elder sister was found to have type IIa hyperlipidemia, while his son had type IV hyperlipidemia. The coexistence of these two types of hyperlipidemia in the same family of K-A-S syndrome has not been reported so far to our knowledge.(ABSTRACT TRUNCATED AT 250 WORDS)

Achilles Tendon↗
PubMed1994

Hyperglycemia as a major determinant of distal polyneuropathy independent of age and diabetes duration in patients with recently diagnosed diabetes.

In an attempt to identify the potential risk factors for diabetic neuropathy in patients recently diagnosed as diabetics, 742 non-insulin-dependent diabetics under 70 years of age who had been diagnosed as diabetics less than 5 years before the initial visit were examined in a cross-sectional study conducted at a university hospital. Neuropathy was defined as the presence of symptoms consistent with distal polyneuropathy, or the absence of tendon reflexes. Of the patients, 21% displayed neuropathy in this study, with no differences between the genders. Age was higher, duration of diabetes was longer, body mass index was lower, and fasting plasma glucose level was higher in patients with neuropathy than in those without neuropathy, for both genders. Body height, maximal body mass index, ethanol use, smoking status, systolic and diastolic blood pressure and serum cholesterol level did not differ between the two groups. Logistic regression analysis showed that fasting plasma glucose level (chi 2 = 28.2) was a major determinant for neuropathy independent of diabetes duration (9.5), age (6.2) and maximal body mass index (3.9). Tight glycemic control from the onset of diabetes was concluded to be essential for the prevention of diabetic distal polyneuropathy.

Adult↗
PubMed1985

Prevalence and pattern of spinocerebellar degenerations in northeastern Libya.

An intensive search over a two-year period for cases of cerebellar and spinocerebellar degenerations in Benghazi, Libya, made through polyclinics, university hospitals and a centre for the handicapped, revealed a total of 52 patients, among whom 30 were index cases; the remainder were detected on family study. Twenty-five patients lived in Benghazi, giving a crude prevalence of 4.8/100 000 population. There were 24 patients (10 families) with hereditary spastic paraplegia (HSP), 13 (9 families) with early onset cerebellar ataxia with retained tendon reflexes (EOCA), 3 with Friedreich's ataxia (FA), 5 (1 family) with late onset cerebellar ataxia (LOCA) with pigmentary retinal degeneration and autosomal dominant inheritance, 6 single cases of LOCA and 1 with ataxia telangiectasia. There were 14 families with definite autosomal recessive inheritance and only 2 with dominant transmission. The large family size (average of 6.2 children per married woman in the patient group) and the high rate of consanguineous marriages contribute to the high incidence of familial cases, especially those with autosomal recessive inheritance. Nerve conduction studies were normal in HSP and abnormal in EOCA and FA. Computed tomographic scans revealed atrophy of the brainstem and cerebellum in 3 cases of EOCA and 2 with LOCA. No indigenous forms of the disease were observed and the clinical features differed little from the descriptions in literature. However, the relative rarity of patients with FA, in comparison with other types of hereditary ataxias, is striking.

Adolescent↗
PubMed1979

Hypocalcemia. Differential diagnosis and mechanisms.

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.

Calcium↗
PubMed1978

Dominant spinopontine atrophy. Report of two additional members of family W.

In five generations of Anglo-Saxon family W, 28 members were affected with dominant hereditary ataxia. In 1969, two members of this family were reported as prototypes of dominant spinopontine atrophy. We discuss two additional members of the original family, with one postmortem examination, including ultrastructual study. In contrast to previously accepted clinical generalizations, we found abolished tendon reflexes and flexion contractures of the lower extremities in patient 1 and onset of illness at the age of 18 years, palatal myoclonus, and optic atrophy in patient 2. Dementia was observed in both patients. Unlike in previous pathological reports, our patient 1 showed definite involvement of the cerebellum and mild degeneration of the inferior olivary nuclei. We conclude, therefore, that clinical and pathological distinction between dominant spinopontine atrophy and olivopontocerebellar atrophy is not clear and raises the question of the justification for regarding dominant spinopontine atrophy as a nosological entity.

Adult↗
PubMed1978

The syndrome of 'continuous muscle fiber activity.'.

A 7-year-old boy who suffered from increasing stiffness and contractures of the extremities had distally pronounced atrophy and absent tendon reflexes. Electromyography showed continuous electrical activity during rest, sleep, after intravenous injection of diazepam, and after peripheral nerve block. The H reflex was elicitable; the silent period after the reflex was absent. Histopathological examination of the peroneus muscle disclosed a marked preponderance of type I fibers and slight atrophy of the type II fibers. Electron microscopic examination of the endplates demonstrated a marked atrophy of the postsynaptic regions and widened synaptic clefts. After one year's treatment with phenytoin, 200 mg daily, the patient showed an almost normal muscle tone. As not all of these electrophysiological phenomena can be fully explained by disturbances of the nerve terminals or the endplates, a further anomaly proximal from the peripheral nerve block seems to have been present.

Child↗
PubMed1981

Pattern reversal visual evoked potentials. Studies in Charcot-Marie-Tooth hereditary neuropathy.

Pattern reversal visual evoked potentials (PRVEP) were studied in 25 patients from 17 separate families with Charcot-Marie-Tooth (CMT) syndrome. Twenty patients had classic CMT with depressed tendon reflexes, slow motor nerve conduction velocities, and autosomal dominant inheritance. Four patients demonstrated typical findings of CMT, but there was no documented family history. One patient had the axonal form of hereditary motor sensory neuropathy. Abnormally delayed latencies of the PRVEP were found in four patients (16% of the total), including the only patient with clinical optic atrophy. There was no consistent correlation, of PRVEP with severity of disease. These results confirm earlier clinical reports of occasional optic nerve involvement in CMT and represent additional evidence that central pathways may be involved in this primarily peripheral nervous system disorder.

Adolescent↗
PubMed1982

Neurotoxic effects of cisplatin therapy.

Swelling of the optic disc and loss of tendon reflexes developed in a 3 1/2-year-old girl after 11 high-dose courses of cisplatin (cis-dichlorodiammine platinum [II]) therapy for recurrent sacrococcygeal teratoma. Postmortem examination demonstrated optic disc swelling; the spinal cord showed loss of myelinated fibers and gliosis of the dorsal columns. To our knowledge this case is the first in which the neuropathologic changes associated with cisplatin therapy have been demonstrated by postmortem examination.

Child, Preschool↗
PubMed1984

Painful ataxic hemiparesis.

Right hemiparesis with right-sided pain and ataxia developed in a 68-year-old man. Sensation, neuropsychological function, and somatosensory evoked potentials were normal. Computed tomography showed an isolated fresh infarct in the left part of the thalamus. The pain and ataxic disturbances were related to involvement of the thalamus itself, but the hemiparesis with hyperactive tendon reflexes and Babinski's sign was probably due to associated dysfunction in the adjacent internal capsule from compression or edema. In the available clinicopathological reports of cases with hemiparesis and thalamic infarction, contiguous involvement of the internal capsule or no associated lesion has been reported. Because of the occurrence of pain, which is not present in pontine, mesencephalic, or capsular ataxic hemiparesis, we suggest that the syndrome seen in our patient be called "painful ataxic hemiparesis."

Ataxia↗
PubMed1992

Cerebral glucose utilization in motor neuron disease.

Positron emission tomography with fluorodeoxyglucose F 18 (18F-fluorodeoxyglucose) was used to examine regional cerebral glucose metabolism in individuals with motor neuron disease. Motor neuron disease involves selective loss of motor neurons, large pyramidal cells in the motor cortex, and corticospinal tract degeneration. We postulated that the local cerebral metabolic rate of glucose should correlate with this regional neuronal cell loss. Glucose metabolism values in patients with motor neuron disease were reduced compared with those of controls in several regions; however, when corrected for multiple comparisons, no significant difference was observed between patients with motor neuron disease and age-matched controls. No correlation was noted between the local cerebral metabolic rate of glucose and duration or severity of illness. Correlation between metabolic changes with objective findings on neurologic examination, including motor weakness and tendon reflexes, provided interesting results, including a decline in glucose metabolism with progressive weakness and upper motor neuron dysfunction. Moreover, in supplementary motor areas, there appears to be an increase in regional glucose metabolism as the neurologic condition deteriorates, possibly representing increased metabolic activity of the motor association cortex in response to primary loss of pyramidal cells.

Adult↗