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Declaration of brain death in neurosurgical and neurological practice.

A survey of neurosurgeons and neurologists assessed physician practices in the declaration of brain death. Ninety-four per cent of the respondents thought that the diagnosis of brain death was legitimate; most thought that it was justified by a failure of somatic survival after brain death. Fifty-four per cent of the respondents had made the diagnosis themselves 1 to 5 times a year. The criteria used to make the diagnosis varied significantly among the respondents. Most required the absence of a pupillary reflex (88%), the absence of a corneal reflex (85%), a lack of ventilatory effort with disconnection of the ventilator (84%), and the absence of eye movements with head turning (80%). Fewer required an absent cough reflex (61%) or gag reflex (69%), dilated pupils (59%), a body temperature under 90 degrees F (56%), or a blood barbiturate level of zero (43%). Over 65% required an isoelectric electroencephalogram; 29% required only one, and 36% required two electroencephalograms 24 hours apart. Twenty-six per cent required absent deep tendon reflexes. The time required for the declaration varied from 6 to 24 hours. There was wide variation in the response to a hypothetical situation in which the family of a patient fulfilling brain death criteria did not want death to be declared. Seventy-eight per cent of the respondents would continue ventilatory support, although about a third of these would declare the patient dead while doing so. Only 6% would stop the ventilator despite the family's wishes. These results substantiate a wide variation in the actions of neurologists and neurosurgeons in brain death declaration. This has important implications for decisions about death in neurology and neurosurgery.

Attitude of Health Personnel↗

[Usefulness of the blink reflex in a case of brainstem neuro-Behcet's disease].

INTRODUCTION: Brainstem is the most frequently affected structure in neurobehçet disease. Brainstem auditory evoked responses (BAER) and magnetic resonance imaging (MRI) have been employed in early diagnosis of the disease. We present here a case of neurobehçet disease which brainstem lesion was suspected by blink reflex and corroborated by MRI. BAER were normal in this case. CLINICAL CASE: The patient was a woman, 49 years old, diagnosed from Behçet's disease. Clinical symptoms consisted of dizziness, headache, nausea, vomiting and bilateral tinnitus preceded by fever in the previous days. Neurological examination showed increased tendon reflexes and adiadochokinesis. Cerebrospinal fluid was inflammatory but aseptic. Computerised tomography and BAER were normal. Blink reflex recording showed abnormalities after the stimulation of the right supraorbital nerve in R2 component, ipsilateral and contralateral, the remainder components being normal. This finding was compatible with a lesion in the spinal tract-nucleus of the right trigeminal nerve. Cranial MRI showed several areas of high signal intensity in protuberancial calotte and spinal tract-nucleus of the trigeminal nerve. The patient improved after prednisone and chlorambucil combined therapy. Serial blink reflex studies were normal, while the patient was asymptomatic. CONCLUSION: These results indicate that determination of blink reflex together with BAER may be of help in the evaluation of a more extensive area of the brainstem in neurobehçet's disease, even in absence of trigemino-facial symptomatology. Early diagnosis is important because of neurobehçet's morbi-mortality.

Behcet Syndrome↗

Clinical utility of reflex studies in assessing cervical radiculopathy.

We prospectively studied the diagnostic utility of upper limb segmental reflexes in patients with suspected cervical radiculopathy (CR). Fifty-three patients (29 men and 24 women), referred for electrodiagnostic testing, were positive for at least one of four clinical criteria for CR: abnormal (1) history, (2) motor (myotomal) examination, (3) sensory (dermatomal) examination, and (4) changes in deep tendon reflexes (DTR). All underwent electrodiagnostic assessment, needle electrode examination (NEE), specialized segmental reflexes (heteronymous and Hoffman's reflexes [H reflexes]), and neuroimaging. The clinical diagnosis was supported in all 32 patients who entered the study with two or more clinical signs for CR. Abnormal NEE was found in 90% of subjects with three clinical signs, 59% with two signs, and only 10% of those with one sign. H reflexes demonstrated a sensitivity of 72% and specificity of 85% for detection of CR and were particularly helpful when forming conclusions in the 21 subjects with only one clinical sign for CR. Specialized segmental H-reflex studies of the upper limb were as sensitive and specific as neuroimaging (magnetic resonance imaging).

Adult↗

Magnesium sulfate in eclampsia and pre-eclampsia: pharmacokinetic principles.

Magnesium sulfate (MgSO4) is the agent most commonly used for treatment of eclampsia and prophylaxis of eclampsia in patients with severe pre-eclampsia. It is usually given by either the intramuscular or intravenous routes. The intramuscular regimen is most commonly a 4 g intravenous loading dose, immediately followed by 10 g intramuscularly and then by 5 g intramuscularly every 4 hours in alternating buttocks. The intravenous regimen is given as a 4 g dose, followed by a maintenance infusion of 1 to 2 g/h by controlled infusion pump. After administration, about 40% of plasma magnesium is protein bound. The unbound magnesium ion diffuses into the extravascular-extracellular space, into bone, and across the placenta and fetal membranes and into the fetus and amniotic fluid. In pregnant women, apparent volumes of distribution usually reach constant values between the third and fourth hours after administration, and range from 0.250 to 0.442 L/kg. Magnesium is almost exclusively excreted in the urine, with 90% of the dose excreted during the first 24 hours after an intravenous infusion of MgSO4. The pharmacokinetic profile of MgSO4 after intravenous administration can be described by a 2-compartment model with a rapid distribution (a) phase, followed by a relative slow beta phase of elimination. The clinical effect and toxicity of MgSO4 can be linked to its concentration in plasma. A concentration of 1.8 to 3.0 mmol/L has been suggested for treatment of eclamptic convulsions. The actual magnesium dose and concentration needed for prophylaxis has never been estimated. Maternal toxicity is rare when MgSO4 is carefully administered and monitored. The first warning of impending toxicity in the mother is loss of the patellar reflex at plasma concentrations between 3.5 and 5 mmol/L. Respiratory paralysis occurs at 5 to 6.5 mmol/L. Cardiac conduction is altered at greater than 7.5 mmol/L, and cardiac arrest can be expected when concentrations of magnesium exceed 12.5 mmol/L. Careful attention to the monitoring guidelines can prevent toxicity. Deep tendon reflexes, respiratory rate, urine output and serum concentrations are the most commonly followed variables. In this review, we will outline the currently available knowledge of the pharmacokinetics of MgSO4 and its clinical usage for women with pre-eclampsia and eclampsia.

Animals↗

Neurophysiological effects of prolonged cooling of the calf in patients with complete spinal transection.

The neurophysiological effects of prolonged cooling were examined in seven patients with complete spinal lesions. The twitch tension of the soleus muscle, the direct (M-wave) and relfex (H-wave) response to electrical stimulation of the popliteal nerve, the Achilles tendon reflex (ATR) and the degree of inhibition of the H-wave by muscle vibration were recorded before and after a minimum of forty-five minutes cooling of the calf. Changes in the configuration of the M-wave occurred, suggesting that cooling results in slowing of conduction in muscle or motor nerve fibers. Prolongation of the twitch contraction and half relaxation time was observed, implying that the contractile mechanism of the muscle is affected. A significant decrease in the ATR/M ratio was observed, indicating that cooling, in addition, affects the muscle spindle or its connections. No significant alterations in the H/M ratio or in the degree of suppression of the H-wave by vibration were observed.

Achilles Tendon↗

Soleus H-reflex tests and clinical signs of the upper motor neuron syndrome.

Soleus H-reflex tests are used for elucidating pathophysiological mechanisms in motor control. The cumulative vibratory inhibition of the soleus H-reflex, the ratio of the reflex to direct muscle potential (H to M ratio) and the recovery curve of the soleus H-reflex were studied in 38 patients with varying signs of the upper motor neuron syndrome for a possible relation with clinical features. The results were compared with those obtained from a group of healthy volunteers. The magnitude of vibratory inhibition decreased with increase of hypertonia. The H to M ratio increased as the activity of the tendon reflex was enhanced and correlated to a lesser degree with muscle tone. Both the H to M ratio and late facilitation of the soleus H-reflex recovery curve were elevated in clonus. The findings suggest that alterations in the results of soleus H-reflex tests relate to specific clinical features of the upper motor neuron syndrome. Possible pathophysiological implications are discussed.

Adolescent↗

Soleus H-reflex recruitment is not altered in persons with chronic spinal cord injury.

OBJECTIVE: To determine whether spasticity in persons with spinal cord injury (SCI) is associated with elevated monosynaptic reflex excitability. DESIGN: One-way experimental. SETTING: Research laboratory. PARTICIPANTS: Convenience sample of 9 subjects (8 men, 1 woman) with chronic and complete SCI and 20 persons (14 men, 6 women) with no neurologic impairment. Subjects with SCI exhibited lower-extremity spasticity as indicated by velocity-dependent increased resistance to passive muscle stretch, abnormally brisk deep tendon reflexes, involuntary lower-extremity flexion and/or extension spasms, and clonus. INTERVENTION: Soleus H-reflex recruitment curves were elicited in all subjects. MAIN OUTCOME MEASURES: Soleus H-reflex threshold (HTH), gain (HGN), and amplitude (HPP). RESULTS: There was no difference between subjects with and without SCI in HTH, HGN, or HPP. CONCLUSIONS: Spasticity in people with chronic and complete SCI was not associated with increased excitability of the connections between Ia afferent projections and motoneurons. Factors extrinsic to these connections may have a role in spasticity caused by SCI.

Adult↗

Functional sparing of intrafusal muscle fibers in muscular dystrophies.

In a previous study, we showed that patients with muscular dystrophies (MDs) perceive passive movements, experience sensations of illusory movement induced by muscle tendon vibration, and have proprioceptive-regulated sways in response to vibratory stimulation applied to the neck and ankle muscle tendons. These findings argue for preserved proprioceptive functions of muscle spindles. However, it is unclear whether the function of intrafusal muscle fibers is spared, i.e., whether they retain their ability to contract when submitted to a fusimotor drive. To answer this question, we analyzed the effects of reinforcement maneuvers (mental computation and the Jendrassik maneuver) that are known to increase muscle spindle sensitivity via fusimotor drive in healthy subjects. Nine patients with different MDs participated in the study. Reinforcement maneuvers increased both the mean amplitude of the Achilles tendon reflex (187 +/- 52.9% of the mean control amplitude) and the sensitivity of muscle spindle afferents to imposed movements of the ankle. The same reinforcement maneuvers failed to alter the amplitude of the Hoffmann reflex in the triceps surae muscle. These results suggest that the intrafusal muscle fibers preserve their contractile abilities in slowly progressive MDs. The reasons for a differential impairment of intrafusal and extrafusal muscle fibers and the clinical implications of the present results are discussed.

Achilles Tendon↗

Depression of fast axonal transport in axons demyelinated by intraneural injection of a neurotoxin from K. humboldtiana.

Tullidinol, a neurotoxin extracted from the Karwinskia humboldtiana fruit, dissolved in peanut oil was injected into the right sciatic nerve of adult cats. The contralateral sciatic nerve received an equivalent volume of peanut oil alone. The fast axonal transport of labeled ([3H]Leucine) protein was studied in sensory and motor axons of both sciatic nerves. The radioactive label was pressure injected either into the L7 dorsal root ganglion or the ventral region of the same spinal cord segment. Several days after the toxin injection, the cat limped and the Achilles tendon reflex was nearly absent in the right hind limb. The amount of transported label was decreased distal to the site of toxin injection. Proximal to this site, the transported material was damned. Sensory and motor axons showed similar changes. In addition, the toxin produced demyelination and axonal degeneration. Axonal transport and the structure of the axons were normal in the contralateral nerve. Both, Schwann cells and axons of the right sciatic nerve showed globular inclusions, presumably oil droplets containing the toxin. We conclude that Schwann cells and axons as well are tullidinol targets.

Achilles Tendon↗

Metabolic insufficiency as a limiting factor in the dietetic treatment of obesity.

Previous observations that acute total fasting decreases serum T3 and increase rT3 has prompted the following study. 17 obese women were placed on a 1000 kcal/day weight-reducing diet, and body weight (BW), serum T4, RT3U, T3, rT3, TSH and the Achilles tendon reflex (ATR) were estimated before and after each month for 3 consecutive months of the diet. The results showed a consistent decrease in serum T3, and inconsistent increase in rT3, a consistent prolongation of the ATR and a levelling-off of the BW loss after the second month of the diet. At 3 months there was a negative correlation between the decrease in BW and the increase in ATR, i.e. the more abnormal the ATR became, the less weight the patient lost. It is concluded: 1) Even a moderate hypocaloric diet in ambulatory patients induces a disturbance in the peripheral conversion of T4 to T3 and a secondary state of metabolic insufficiency. 2). This insufficiency is probable related to the observed tendency of the BW loss to level off after two months. 3) A controlled trial of physiologic doses of T3, such as 40 mu g/day, seems indicated, as opposed to pharmacologic dosed of T3 used by previous investigators.

Achilles Tendon↗

Neurophysiological changes following spinal cord lesions in man.

A study has been made of the neurophysiological changes that follow spinal cord lesions in man. The Achilles tendon reflex (ATR) is used to estimate transmission in the Ia monosynaptic pathway, and the tonic vibration reflex (TVR) to estimate transmission in the Ia polysynaptic pathway to motoneurons. The inhibition of the H reflex by vibration is used as an estimate of presynaptic inhibition of the Ia monosynaptic pathway. Immediately following a complete lesion of the spinal cord presynaptic inhibition of the Ia monosynaptic pathway appears to be greatly increased. This enhanced inihibition may last several months but it eventually declines and in some instances becomes less than normal. Transmission in the Ia polysynaptic pathway is permanently abolished by a complete spinal lesion. A hypothesis is developed from these findings to explain the evolution of some of the clinical features that follow complete spinal lesions in man. Distinct differences are observed when the spinal lesion is incomplete. Transmission in the Ia polysynaptic pathway may be preserved and there may be no increase in presynaptic inhibition. These differences may depend upon the integrity of certain spinal long tracts which cannot be tested clinically.

Achilles Tendon↗

Risk factors predicting lower extremity amputations in patients with NIDDM.

OBJECTIVE: To examine the predictors of lower extremity amputation in patients with NIDDM. RESEARCH DESIGN AND METHODS: At baseline, risk factors for amputation were determined in 1,044 NIDDM patients (571 men, 473 women) aged 45 to 64 years. These patients were followed up to 7 years with respect to amputation. RESULTS: The incidence of amputation was 5.6% in men and 5.3% in women. High fasting plasma glucose at baseline examination and the duration of diabetes were associated with a twofold risk for amputation. Similarly, glycemic control measured at baseline by HbA1 was an important predictor of amputation. There was a dose-response relationship between plasma glucose or HbA1 and the risk for amputation. The effect of hyperglycemia on the risk of amputation was seen clearly even after the adjustment for other cardiovascular risk factors. Signs of peripheral neuropathy and bilateral absence of Achilles tendon reflexes and vibration sense were important predictors for amputation. Furthermore, absent peripheral artery pulses and femoral artery bruit on auscultation predicted amputation. CONCLUSIONS: Our 7-year follow-up study gives strong evidence that poor glycemic control is an important predictor of amputation in patients with NIDDM in addition to clinically detectable peripheral arterial disease and peripheral neuropathy.

Achilles Tendon↗

Stretch- and H-reflexes of the lower leg during whole body cooling and local warming.

BACKGROUND: This study was undertaken to evaluate if possible changes in stretch- and H-reflexes could be related to the changes in the EMG activity of the cooled lower leg muscles observed during a stretch-shortening cycle exercise. METHODS: Eight subjects wearing shorts and jogging shoes were exposed once to 27 degrees C and twice to 10 degrees C for 60 min each. During the second exposure to 10 degrees C, the subject's lower legs were kept warm (10 degrees Clw) with electrical pillows. After the exposures Achilles tendon reflex (stretch reflex) was induced and the EMG activity of the triceps surae was measured. Immediately after reflex measurements the EMG activity of the triceps surae and tibialis anterior during a drop-jump (stretch-shortening cycle) was measured. After similar thermal exposures electrically induced H-reflex from the calf was measured. RESULTS: During the preactivity and stretch phases the EMG activity of the triceps surae increased after the exposure to 10 degrees C, whereas during the shortening phase it decreased. During the shortening phase cooling, on the contrary, increased the activity of tibialis surae anterior. These changes disappeared at 10 degrees Clw. At 10 degrees C the maximum EMG-amplitude of triceps surae during stretch reflex decreased (p<0.05), reflecting suppressed muscle spindle activity. Suppressed spindle activity causes the agonist to be unfacilitated and the antagonist muscle contraction to be uninhibited, which was seen in the present study as decreased agonist and increased antagonist EMG activity during the shortening phase at 10 degrees C. The Hmax/Mmax-ratio, H-reflex latency and amplitude increased at 10 degrees C (p<0.05), reflecting increased motoneuron pool excitability. This in part may explain the increased EMG activity during the preactivity and stretch phases. CONCLUSION: Cooling-induced increase in the excitability of the motoneuron pool and suppression of muscle spindle activity seem to be responsible of the EMG activity changes during the stretch-shortening cycle, consequently decreasing muscular performance.

Adult↗

["Skip lesions" in neurological deficits caused by tethered cord syndrome].

The neurological deficits caused by tethered cord syndrome do not necessarily follow a dermatomal pattern of the affected spinal cord from caudal to cephalic fashion. The authors defined these neurological deficits as "skip lesions", and reviewed the neurological deficits in tethered cord syndrome. Among 29 cases, inconsecutive segmental motor weakness in 3 cases, inconsecutive segmental sensory impairment in 6 cases, positive Babinski reflex in 8 cases, supranuclear neurogenic bladder in 3 cases and lumbago or leg pain in 4 cases were observed and they were thought to be compatible with the neurological deficits called "skip lesions". The basic mechanism of this sign is that the cephalic portion of the spinal cord is functionally impaired during flexion of the lumbosacral spine, while the caudal spinal cord with decreased visco-elasticity dose not elongate. Inconsecutive motor-sensory disturbance, accelerated deep tendon reflexes in the lower extremities, positive Babinski or other pathological reflexes in the lower extremities, uninhibited neurogenic bladder, lumbago and pain in the legs were considered to belong to the category of "skip lesions" and they can be treated by the untethering procedure. The authors concluded that preoperative careful insight into the mechanism of "skip lesions" revealed surgical efficacy for the reversible neurological deficits by the untethering procedure, or the efficacy of decompression of the lipoma or neurolysis around the involved spinal nerve roots.

Humans↗

Changes of triiodothyronine and thyroxine in patients with thyrocardiac disease and their relationship to systolic time intervals.

The relationship between the ejection time from the left ventricle (LVET), the pre-ejection period (PEP) of the left ventricle, the Q-Kd interval, the course of the Achilles tendon reflex (ATR) and the thyroxine (T4) and triiodothyronine (T3) serum level in 184 patients with different grades of thyroid function was investigated. Some of these patients suffered from cardiac affection caused by thyrotoxicosis or ischemic heart disease. The significant inverse correlations between the T3 level and the duration of PEP, LVET, the Q-Kd interval and the ATR was revealed. An inverse relationship with T4 level was found only in the Q-Kd interval and ATR. In those instances, where there was a correlation with T4 and T3, higher values of correlation coefficients were observed in the correlation with T3. T4 concentration was higher in patients with cardiac affection. In thyrocardiacs was an increase in the quotient T4:T3, while in thyrotoxic patients without cardiac affection this quotient was rather decreased. The significance of disturbed T4 metabolism in development of cardiac affection in thyrotoxicosis is discussed with respect to ageing processes.

Achilles Tendon↗

Muscle-nerve involvement in autosomal dominant progressive external ophthalmoplegia with hypogonadism.

Sixteen members of a family with a history of autosomal dominant progressive external ophthalmoplegia (adPEO) with hypogonadism were examined. The muscular involvement commenced cranially and descended in relation to increasing disease duration. The neuromuscular signs were PEO, dysarthria, dysphonia, limb muscle weakness with wasting, absence of Achilles tendon reflexes, and distal vibration sensory loss. The electromyogram (EMG) was myopathic in facial and proximal limb muscles. Neurogenic involvement was suspected in a few tibial anterior muscles. Neurography showed signs of axonal neuropathy correlated to clinical signs. F-responses were reduced in number or absent in peroneal nerves, and did not correlate to clinical signs or disease duration. Muscle biopsies in advanced cases had structural abnormalities of mitochondria, ragged-red fibers, and focal cytochrome c oxidase deficiency. A combination of muscle-nerve involvement with PEO, Achilles tendon areflexia, distal vibration sensory impairment, myopathic EMG, and abnormally low sural nerve responses seems to be typical of this type of mitochondrial disorder.

Adolescent↗

Changes in motor activity and biomechanics during balance recovery following cutaneous and muscular deafferentation.

The effects of lower limb deafferentation were examined during execution of a balance recovery step following a forward fall induced by release of an initial inclined posture. The subjects were healthy control subjects and patients with a unilateral loss of the Achilles tendon reflex following S1 radiculitis. Deafferentation of healthy subjects was obtained by unilateral leg ischemia (four subjects) and by foot anesthesia (five subjects). The balance recovery step was characterized by the surface electromyographic (EMG) activity of right and left soleus and tibialis anterior muscles and the kinetics of the center of gravity and center of foot pressure. Experimentally induced and pathological deafferentation decreased the EMG activity of the ipsilateral soleus and lowered the vertical ground reaction force. The lower limb motor activity was more affected by loss of muscle proprioceptive afferents than by loss of plantar cutaneous afferents. Patients showed early and bilateral changes in soleus and tibialis activities, whichever side was affected. The step length of patients was also shorter than that of controls, but it remained similar before and after deafferentation in the healthy subjects. The results are discussed in terms of ipsilateral and crossed pathway connections and functional adaptive strategies.

Achilles Tendon↗

[A case of chronic progressive external ophthalmoplegia with Oguchi's disease].

A 52-year-old case of chronic external ophthalmoplegia accompanied by Oguchi's disease was reported. The patient noticed night blindness and deafness since childhood. Later he developed ocular movement limitation to all directions by the age of 40. He had 20/20 corrected visual acuity and normal anterior segment, as well as normal color vision. Goldmann's perimetry showed generalized constriction of the peripheral field. Golden tapetal reflex without dark adaptation disappeared after 4 hours of dark adaptation, i.e. Mizuo-Nakamura's phenomenon was recognized. Recovery of diminished a and b wave electroretinogram to the subnormal range was also observed after 4 hours of dark adaptation. Rod-cone interaction test revealed a monophasic adaptation, and no suppression to the cones from the rods was observed. This finding was also compatible with Oguchi's disease. ECG revealed incomplete atrio-ventricular as well as right bundle branch blocks. Neurological examination findings were entirely normal other than slight enhancement of deep tendon reflexes in the lower extremities and mixed typed difficulty of hearing. Muscle biopsy of the right medial rectus muscle revealed ragged-red fiber, suggesting mitochondrial abnormalities. Never the less the quadriceps femoris muscle biopsy specimen showed normal histological findings. This is the first case report of progressive external ophthalmoplegia associated with Oguchi's disease. Mitochondrial abnormality was confirmed only in the external ocular muscle. This case may be a variant of Kearns-Sayre syndrome.

Humans↗