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PubMed1993

Examination of distal involvement in cisplatin-induced neuropathy in man. An electrophysiological and histological study with particular reference to touch receptor function.

Cisplatin is a widely used anti-neoplastic agent with dose-dependent sensory neuropathy as a major side-effect. The mechanism for the neuropathy is poorly understood; it may be caused by a lesion of the dorsal root ganglion cells or by a distal axonopathy. This distinction is important since regeneration in a neuronopathy is impossible, whereas recovery may occur if the axon is affected only distally. The most distal part of the sensory nerve fibre is, however, not accessible for conventional electrophysiological examination. To ascertain whether the distal receptor-associated part of the fibre is involved, we have used a method previously untested in patients with neuropathy. In 26 males treated with cisplatin for testicular cancer 3-6.5 years previously, and in 22 normal males, the compound sensory action potentials evoked by a tactile probe were recorded through needle electrodes placed close to the sural and median nerves. The responses were compared with action potentials evoked by electrical stimulation of the same nerves. Biopsies from the distal sural nerve at the dorsolateral aspect of the foot were obtained in three patients and in four subjects not treated with cisplatin. Sixteen patients had received a conventional dose (307-435 mg/m2) of cisplatin and 10 patients had received a high dose (553-1197 mg/m2). Two-thirds of the conventional dose patients and all the high dose patients had mild to severe sensory loss and reduced or absent tendon reflexes. The amplitude of the electrically evoked sensory action potential decreased with increasing dose of cisplatin and was correlated with the reduction of vibration sense. Tactile responses, probably originating mainly from Pacinian corpuscles, were, with the exception of two high dose patients, recorded from all sural and median nerves. The two high dose patients without a tactile response had a severely reduced or no electrically evoked response at the sural nerve. The sural nerve biopsies from high dose patients showed loss of large fibres; Pacinian corpuscles were obtained in two of these patients and contained normal axons. Our findings do not suggest that cisplatin causes a primarily distal lesion with sparing of more proximal parts of the peripheral nerve. We interpret the results as being consistent with a neuronopathy affecting primarily large sensory neurons. Brainstem and somatosensory evoked potentials and H-reflexes suggested that the spinal cord and brainstem were affected as well.

Action Potentials↗
PubMed1993

Longitudinal study of central motor conduction time following stroke. 2. Central motor conduction measured within 72 h after stroke as a predictor of functional outcome at 12 months.

A longitudinal study was performed on 118 first-ever stroke patients to evaluate neurophysiological measurements of central motor conduction time (CMCT) in the period immediately following stroke as predictors of functional outcome and mortality at 12 months. Measurements of CMCT were made as described in the accompanying article (Heald et al., 1993, Brain, 116, 1355-1370), in which the following three groups of patients were recognized within 12-72 h after the onset of symptoms: normal response group, delayed response group and no response group. Neurophysiological and clinical investigations were commenced 12-72 h (designated as day 1) after the onset of symptoms and repeated at set time intervals up to 12 months. The subjects were examined neurologically and assessed using the Motricity Index for muscle strength, the Nine-hole Peg Test to measure manual dexterity, the Barthel Score for activities of daily living and the modified Rankin Scale for functional outcome. The duration of stay in hospital and the occurrence of stroke-related death were noted. During the first week following stroke, absence of responses correlated closely with the patient's symptoms and neurological observations of abnormal muscle tone and tendon reflexes. Correlations were made in the three groups of patients of functional scores at day 1 and at 12 months. Patients with normal CMCT had consistently higher scores throughout the 12 month period and achieved significantly better functional recovery. Patients with no responses showed poor performance in neurological and functional tests throughout the 12 month period. Patients with delayed CMCT had neurological and functional scores intermediate between those of the other two groups, but outcome at 12 months was similar to those in the normal response group. Where the threshold to cortical stimulation was abnormally high, functional outcome was generally poor. Mortality was highest in the group with absent responses and the survivors spent the longest period in hospital. In conclusion, the observation of normal or delayed CMCT at day 1 identifies a group of patients with a high probability of survival and functional recovery. The absence of responses to cortical stimulation at day 1 identifies a group of patients who are at high risk of poor functional recovery at 12 months and greater probability of stroke-related death during this period.

Cerebrovascular Disorders↗
PubMed1993

Phenotypic variability in autosomal dominant cerebellar ataxia type I is unrelated to genetic heterogeneity.

Families with autosomal dominant cerebellar ataxia (ADCA), a heterogeneous group of diseases, were investigated prior to and during genetic linkage analysis. We report here on the clinical features of 122 affected individuals from 36 unrelated families with ADCA type I, the most common type. Our results indicate an anticipation expressed in a mean 9.4 year earlier age at onset and more rapid clinical progression in successive generations. There was no imprinting, since age at onset, disease duration and severity of the disease were independent of parental transmission. Progressive cerebellar ataxia was variably associated with signs such as ophthalmoplegia, dysphagia, sphincter disturbances, briskness or loss of tendon reflexes, decreased vibration sense and amyotrophy, a variability correlated with disease duration. Linkage analysis of 10 informative families with microsatellite markers, located on the short arm of the chromosome 6, allowed the identification of four families showing positive linkage to the SCA1 (spinal cerebellar ataxia 1) locus and six non-SCA1 families for whom linkage to this locus was excluded. This reflects non-allelic genetic heterogeneity. Thus, the analysis of clinical signs associated with cerebellar ataxia in SCA1 versus non-SCA1 kindreds did not distinguish between the two groups. The clinical picture of ADCA type I did not reflect the genetic heterogeneity of the disease.

Adolescent↗
PubMed1998

The role of the SCA2 trinucleotide repeat expansion in 89 autosomal dominant cerebellar ataxia families. Frequency, clinical and genetic correlates.

The spinocerebellar ataxia type 2 (SCA2) is caused by a trinucleotide (CAG) expansion in the coding region of the ataxin 2 gene on chromosome 12q.89 families with autosomal dominant cerebellar ataxia (ADCA) types I, II and III, and 47 isolated cases with idiopathic late onset cerebellar ataxia (ILOCA), were analysed for this mutation. The identification of the SCA2 mutation in 31 out of 38 families with the ADCA I phenotype, but in none of those with ADCA II, ADCA III or ILOCA confirms the specificity of this mutation. A clinical comparison of the ADCA I patients with the three known mutations (SCA1, -2 or -3) highlights significant differences between the groups; SCA2 patients tended to have a longer disease duration, a higher frequency of slow saccades and depressed tendon reflexes. However, these neurological signs were also seen in an ADCA I family in which the SCA2 mutation was not identified, illustrating the importance of a direct genetic test. The SCA2 families were from different geographical and ethnic backgrounds. However, haplotype analysis failed to show evidence of a founder mutation, even in families from the same geographical origin. The range of normal alleles varied from 17 to 30 CAG repeats and from 35 to 51 repeats for the pathological alleles. Similar to the other diseases caused by unstable trinucleotide repeats, a significant inverse correlation has been found between the number of repeats and age of onset, and there is a significantly higher paternal instability of repeat length on transmission to offspring. The SCA2 mutation is the most frequent amongst ADCA I patients, accounting for 40%, compared with SCA1 and SCA3 which account for 35% and 15%, respectively.

Adolescent↗
PubMed2000

Phenotypic and genotypic heterogeneity in hereditary motor neuronopathy type V: a clinical, electrophysiological and genetic study.

We report on a large four-generation Austrian family with autosomal dominant distal hereditary motor neuronopathy type V (distal HMN V). Forty-seven at-risk family members, of whom 21 were definitely affected, underwent detailed clinical, electrophysiological and genetic studies. The age at onset was in the second decade of life in most affected individuals, but clinical presentation was rather variable. While the majority of patients were primarily disabled by progressive asymmetrical wasting of the thenar and the first dorsal interosseus muscles, others had marked foot deformity and gait disturbance with the occasional absence of hand involvement. Sensation sense was normal except for the reduced response to vibration. Many individuals showed brisk tendon reflexes and some elevated muscle tone in the lower limbs, but extensor plantar responses were rarely observed. Electrophysiological evaluation revealed normal or reduced motor nerve conduction velocities, normal or prolonged distal motor latencies, and low compound motor action potentials, depending on the degree of muscle wasting. Sensory nerve studies were usually within the normal range or slightly to moderately abnormal in older or severely affected persons. Electromyography showed high-amplitude motor unit potentials and reduced recruitment compatible with anterior horn cell degeneration. Central motor conduction times were prolonged in two-thirds of the patients. Molecular genetic studies excluded Charcot-Marie-Tooth 1A syndrome and proximal spinal muscular atrophy linked to chromosome 5q as well as the known gene loci for distal HMN II on chromosome 12q, HMN V on chromosome 7p and juvenile amyotrophic lateral sclerosis on chromosome 9q. The findings in this family thus provide detailed clinical and electrophysiological information on HMN V and demonstrate broad phenotypic variability in this disorder. Hallmark features are discussed that appear to be most reliable to differentiate this type of HMN V from other variants of hereditary neuropathies, and a set of diagnostic criteria is proposed. Furthermore, this is the first report of prolonged central motor conduction times in HMN V, which indicates additional involvement of the central motor pathways in this disease. Finally, molecular genetic studies demonstrate genetic heterogeneity, suggesting the existence of at least a second genetic subtype in HMN V.

Adolescent↗
PubMed2004

Reciprocal inhibition and corticospinal transmission in the arm and leg in patients with autosomal dominant pure spastic paraparesis (ADPSP).

The pathophysiological mechanisms underlying the development of spasticity are not clear, but the excitability of the disynaptic reciprocal inhibitory pathway is affected in many patients with spasticity of different origin. Patients with genetically identified autosomal dominant pure spastic paraparesis (ADPSP) develop spasticity and paresis in the legs, but usually have no symptoms in the arms. Comparison of the spinal and supraspinal control of the legs and arms in these patients may therefore provide valuable information about the pathophysiology of spasticity. In the present study, we tested the hypothesis that one of the pathophysiological mechanisms of spasticity in these patients is abnormal corticospinal transmission and that this may lead to decreased reciprocal inhibition. Ten patients and 15 healthy age-matched control subjects were investigated. The patients were all spastic in the legs (with hyperactive tendon reflexes, increased muscle tone and Babinski sign), but had no neurological symptoms in the arms (except for one patient). Disynaptic reciprocal Ia inhibition of flexor carpi radialis (FCR) and soleus (SOL) motoneurons was measured (as the depression of the background FCR and SOL EMG activity and as the short latency inhibition of the FCR and SOL H-reflex evoked by radial and peroneal nerve stimulation). In addition, the latency of motor evoked potentials (MEPs) in the FCR muscle and the tibialis anterior (TA) muscle was measured. In the patients, the mean reciprocal inhibition was normal in the arms, while it was significantly decreased in the leg compared with the healthy subjects. In the patients, the average latency of MEPs in the FCR muscle was normal, while the latency to the MEP in TA muscle was significantly longer than that found in healthy subjects. Four patients, however, differed from the other patients by having significant reciprocal inhibition in the leg and a significantly shorter latency of TA MEPs than found in the other patients. The six patients without reciprocal inhibition in the leg instead had significant short latency facilitation of the SOL H-reflex and a longer TA MEP latency than seen in the healthy subjects and in the four patients with retained reciprocal inhibition. These findings support the hypothesis that disynaptic reciprocal inhibition and short latency facilitation are involved in the development of spasticity and, furthermore, they suggest a positive correlation between impairment of corticospinal transmission and decrease of reciprocal inhibition/appearance of reciprocal facilitation.

Adult↗
PubMed2005

SCA28, a novel form of autosomal dominant cerebellar ataxia on chromosome 18p11.22-q11.2.

We describe a four-generation Italian family with a novel form of juvenile-onset, slowly progressive, autosomal dominant cerebellar ataxia. Eleven affected family members have been evaluated. The mean age at onset was 19.5 years with no evidence of anticipation. The first symptoms were invariably unbalanced standing and mild gait incoordination. Gaze-evoked nystagmus was prominent at onset, while patients with longer disease duration developed slow saccades, ophthalmoparesis and, often, ptosis. Deep tendon reflexes in lower limbs were increased in 80% of the cases. Genetic analysis excluded the presence of pathological repeat expansions in spinocerebellar ataxia (SCA) types 1-3, 6-8, 10, 12 and 17, and DRPLA genes. Linkage exclusion tests showed no evidence of association with other known SCA loci. A genome-wide screen analysis identified linkage with chromosome 18 markers. A maximum two-point limit of determination score of 4.20 was found for marker D18S53. Haplotype analysis refined a critical region of 7.9 Mb between markers D18S1418 and D18S1104. This new SCA locus on 18p11.22-q11.2 has been designated SCA28. Candidate genes within the critical interval are currently screened for mutations.

Adult↗
PubMed1989

Long-latency enhancement of quadriceps excitability from stimulation of skin afferents in young and old adults.

This study examined the role of cutaneous input on spinal excitability in young and old adults. Patellar tendon reflexes were elicited in 15 old adults (M = 75 yrs) and 25 young adults (M = 26 yrs) at intervals ranging from 15 to 175 ms following cutaneous stimulation to one of four skin sites: (a) ipsilateral calf, (b) contralateral calf (old adults only), (c) ipsilateral anterior thigh, and (d) contralateral anterior thigh. The younger adults had a more vigorous reflex response than the older adults, as indicated by peak force. Force latencies were also faster for the younger adults than the older adults. However, both age groups showed a long-latency facilitation of quadriceps excitability regardless of cutaneous stimulation site. Thus, it seems that low threshold cutaneous afferents contribute an excitatory input to the extensor motoneuron pool that is maintained with age.

Adult↗
PubMed1996

Autosomal dominant Charcot-Marie-Tooth axonal neuropathy mapped on chromosome 7p (CMT2D).

Clinical, electrophysiological and genetic linkage studies were performed on a large autosomal dominant family with Charcot-Marie-Tooth axonal neuropathy type 2 (CMT2) with 38 members of which 14 were affected. Onset of the disease was between 16 and 30 years of age with weakness and atrophy of the hands more severe than of the feet with slow progressive course in 12 patients. Deep tendon reflexes were absent in the upper extremities and decreased in the lower extremities. There was distal hypesthesia for touch, proprioception and vibration sense for the hands more than for the feet. Motor nerve conduction velocities showed normal values (48-53 M/s) with normal latencies (2-3 msec) and electromyography revealed signs of denervation. Genetic linkage analysis used 167 short tandem repeat markers (STRPs) spaced throughout the 22 autosomes. Linkage to the short arm of chromosome 7 at 7p14 was found using the marker D7S435 (Z = 4.83 at theta = 0). Flanking markers were D7S1808 and D7S1806 and the genetic distance between them was 6.8 cM. The multipoint linkage analysis gave a peek multipoint lod score of 6.89 between the markers D7S1808 and D7S435. Linkage analysis showed significantly negative lod scores (with values less than -2) with markers of chromosomes 1 and 3 where CMT axonal forms have been previously mapped. PFGE analysis indicated the absence of the CMT1A duplication. Our findings are consistent with a new genetic type of axonal CMT neuropathy designated by us as CMT2D. Potential candidate genes are multiple T-cell gamma receptor genes which map to the same cytogenetic interval as CMT2D neuropathy.

Charcot-Marie-Tooth Disease↗
PubMed2000

Vincristine-induced dysphagia suggesting esophageal motor dysfunction: a case report.

Transient esophageal motor dysfunction with dysphagia was observed in a 62-year-old man receiving vincristine-containing chemotherapy for non-Hodgkin's lymphoma. Neurological examinations, including muscle strength of extremities, deep tendon reflexes and cranial nerves, were normal. However, the patient complained of severe numbness in the fingertips and toes. The results of esophagogram and esophagoscopy were unremarkable. However, a significantly prolonged esophageal transit time was observed. Vincristine was considered as the causative agent. Empirical vitamin and metoclopramide were prescribed for his neurological symptoms but there was no improvement. The symptoms of dysphagia subsided spontaneously 2 weeks later. However, prompt recurrence of severe dysphagia was observed again after administration of the second and third courses of treatment, which again disappeared upon discontinuation of the drug. Peripheral nerves and the gastrointestinal tract are often affected by vincristine. Common gastrointestinal tract symptoms of vincristine neuropathy may be colicky abdominal pain and constipation. However, vincristine-induced esophageal motor dysfunction with dysphagia is uncommon but generally reversible. The oncologist and chemotherapist should be aware of this complication.

Antineoplastic Agents, Phytogenic↗
PubMed1983

Methyl mercury exposure in northern Quebec. II. Neurologic findings in children.

The relationship between prenatal exposure to methyl mercury and neurologic and developmental abnormalities was ascertained among 234 Cree Indian children aged 12 to 30 months from four northern Quebec communities. A pediatric neurologist, "blinded" to the children's level of exposure, assessed neurologic, physical, mental, and psychosocial development. Methyl mercury exposure was estimated from maternal hair segments representing the period of pregnancy. Abnormality of the tendon reflexes, observed in 13 boys (11 per cent) and in 14 girls (12 per cent), was positively associated with methyl mercury exposure only in boys and there was no consistent dose-response relationship. Other neurologic disorders were less prevalent and none was positively associated with exposure; indeed, incoordination was negatively associated with exposure in girls. The mild, isolated neurologic abnormalities found after prenatal exposure to methyl mercury in northern Quebec were different from the effects of prenatal exposure described in other areas, and their clinical importance can be determined only by continued medical surveillance.

Adult↗
PubMed1990

Sensory neuropathy in non-insulin-dependent diabetes mellitus. The San Luis Valley Diabetes Study.

A screening neurologic examination capable of detecting distal symmetric (sensory) neuropathy in a large population-based study of non-insulin-dependent diabetes mellitus in San Luis Valley, Colorado, in 1984-1986 is described and validated. The examination, completed in 279 diabetics and 577 controls, had 90% agreement with a standard neurologic examination completed on a subsample of 38 patients. Independent validation of neuropathy status was obtained with the Optacon tactile (vibration) stimulator. Mean, age-adjusted vibration threshold was significantly greater in those with neuropathy than in those without. The subtests of the examination most sensitive in detecting neuropathy were a combination of a positive history of neuropathy symptoms and decreased or absent deep tendon reflexes in both ankles. Age-adjusted prevalence of neuropathy in controls, those with impaired glucose tolerance, and diabetics was 3.9%, 11.2%, and 25.8%, respectively. Prevalence odds ratios were 3.5 and 10.6 for the presence of neuropathy in persons with impaired glucose tolerance and diabetes, respectively, compared with persons with normal glucose tolerance. Neuropathy was significantly associated with age, duration of diabetes, male sex, and glycemic control, but not with Anglo/Hispanic status.

Adult↗
PubMed1997

Unusual presentations of hypothyroidism.

Hypothyroidism is a commonly diagnosed endocrine disorder. Typical signs and symptoms of hypothyroidism include lethargy, cold intolerance, hoarseness, dry skin, constipation, delayed relaxation phase of deep tendon reflexes, and bradycardia. Hypothyroidism, presenting with such classic manifestations, usually is readily recognized and, therefore, easy to diagnose. Occasionally patients have less commonly emphasized symptoms, making the diagnosis less apparent. Such atypical presentations may suggest other diseases as the primary problem and, therefore, the initial focus of attention is on a diagnosis other than hypothyroidism. We have observed patients with hypothyroidism with rare manifestations. The diagnosis of primary hypothyroidism was established in all patients by thyroid function tests, and initiation of thyroid hormone therapy resulted in significant improvement of the presenting symptom. We considered it instructive to report about these patients because it shows the need to be aware of the unusual presentations of hypothyroidism and to consider hypothyroidism when confronted with atypical clinical manifestations.

Adult↗
PubMed1981

Studies in the primate on the analgetic effects associated with intrathecal actions of opiates, alpha-adrenergic agonists and baclofen.

The effects of intrathecally administered opiates (morphine sulfate and meperidine), alpha-adrenergic agonists (clonidine and ST-91) and baclofen were examined on the shock titration threshold of macaque monkeys chronically prepared with intrathecal (I) or epidural (E) catheters. Spinal opiates produced a long-lasting analgesia which was antagonized by naloxone. The order of potency was I morphine greater than I meperidine greater than E meperidine greater than E morphine. Clonidine and ST-91, also produced a dose-dependent, long-lasting elevation in the shock titration threshold, antagonized by phentolamine, but not naloxone. L-baclofen, but not D-baclofen, resulted in a dose-dependent elevation of shock titration threshold, which was not antagonized by naloxone. Repeated administration at 24-h intervals over a 7-day period of morphine, clonidine or baclofen, resulted in a significant reduction in the analgetic effects of each drug. Cross tolerance between the three classes of agents was not observed. Intrathecal co-administration of inactive doses of ST-91 and morphine resulted in a near maximal increase in the shock titration threshold, which failed to show any significant tolerance over 21 days. Intrathecal ST-91 and morphine produced no change in either muscle strength, tendon reflexes, respiratory rate, urine formation, or the ability to locomote. Baclofen, in contrast, produced a dose-dependent decrease in muscle strength. That the intrathecal drugs did not produce anesthesia was demonstrated by their failure to block the avoidance response to ensuing ear shock cued by a light tactile stimulus applied to the hind paw. These results clearly indicate that a powerful analgesia can be produced by selectively activating adrenergic, opiate, and baclofenergic receptor systems in the spinal cord.

Adrenergic alpha-Agonists↗
PubMed1995

Phase I safety assessment of intrathecal neostigmine methylsulfate in humans.

BACKGROUND: In dogs, sheep, and rats, spinal neostigmine produces analgesia alone and enhances analgesia from alpha 2-adrenergic agonists. This study assesses side effects and analgesia from intrathecal neostigmine in healthy volunteers. METHODS: After institutional review board approval and informed consent, 28 healthy volunteers were studied. The first 14 volunteers received neostigmine (50-750 micrograms) through a #19.5 spinal needle followed by insertion of a spinal catheter. The remaining 14 volunteers received neostigmine through a #25 or #27 spinal needle without a catheter. Safety measurements included blood pressure, heart rate, oxyhemoglobin saturation, end-tidal carbon dioxide, neurologic evaluation, and computer tests of vigilance and memory. Analgesia in response to ice water immersion was measured. RESULTS: Neostigmine (50 micrograms) through the #19.5 needle did not affect any measured variable. Neostigmine (150 micrograms) caused mild nausea, and 500-750 micrograms caused severe nausea and vomiting. Neostigmine (150-750 micrograms) produced subjective leg weakness, decreased deep tendon reflexes, and sedation. The 750-micrograms dose was associated with anxiety, increased blood pressure and heart rate, and decreased end-tidal carbon dioxide. Neostigmine (100-200 micrograms) in saline, injected through a #25 or #27 needle, caused protracted, severe nausea, and vomiting. This did not occur when dextrose was added to neostigmine. Neostigmine by either method of administration reduced visual analog pain scores to immersion of the foot in ice water. CONCLUSIONS: The incidence and severity of these adverse events from intrathecal neostigmine appears to be affected by dose, method of administration, and baricity of solution. These effects in humans are consistent with studies in animals. Because no unexpected or dangerous side effects occurred, cautious examination of intrathecal neostigmine alone and in combination with other agents for analgesia is warranted.

Adult↗
PubMedDate not supplied

Orally delivered baclofen to control spastic hypertonia in acquired brain injury.

To determine if oral/systemic delivery of baclofen can effectively decrease spastic hypertonia due to acquired brain injury (traumatic brain injury, stroke, anoxia, or encephalopathy). Tertiary care outpatient rehabilitation center directly attached to a university hospital. Patients were a convenience sample recruited consecutively who had been referred for treatment of their spastic hypertonia to our spasticity clinic over a 5-year period. The spastic hypertonia was due to an acquired brain injury by either traumatic brain injury (TBI), stroke, or anoxic brain injury. All patients were more than 6 months postinjury or illness. Retrospective review of patients before and after initiation of treatment with oral baclofen, per standardized clinical data sheets. Thirty-five patients (22 TBI patients) were started on oral baclofen and were reevaluated between 1 to 3 months after initiation of treatment. Data for motor tone (Ashworth scores), spasm scores (Penn spasm frequency score), and deep tendon reflex scores were collected on the affected upper extremity (UE) and lower extremity (LE) side(s). Normal extremities were not assessed. Differences over time were assessed via descriptive statistics and Wilcoxon signed-rank. After 1 to 3 months of treatment when subjects had reached their maximal tolerated dosage, the average LE Ashworth score in the affected lower extremities (LEs) decreased from 3.5 to 3.2 (P =.0003), the reflex score decreased from 2.5 to 2.2 (P =.0274), and there was no statistical difference in the spasm score (P >.05). When the 22 TBI patients are analyzed separately, the average LE Ashworth score decreased from 3.5 to 3.2 (P =.0044) and the reflex score decreased from 2.7 to 2.0 (P =.0003). There was no statistically significant change in UE tone, spasm frequency, or reflexes after 1 to 3 months of treatment (P >.05). The average dosage at follow-up was 57 mg/day of baclofen (range 15-120 mg/day). There was a 17% incidence of somnolence that limited the maximum daily dosage of the medication. The oral delivery of baclofen is capable of reducing LE spastic hypertonia resulting from acquired brain injury. The lack of effect upon the upper extremities may be due to receptor specificity issues. GABA-B receptors may be less involved in the modulation of UE spastic hypertonia.

Administration, Oral↗
PubMed2003

Comparative neurotoxicity of weekly non-break paclitaxel infusions over 1 versus 3 h.

We evaluated the effects of weekly short infusions of paclitaxel (PAC) on the development of a peripheral neuropathy (PNP) as primary endpoint. Patients with advanced cancer were randomized to a weekly regimen of PAC (100 mg/m2) infused over 1 versus 3 h. PNP was evaluated by a clinical score including sensory symptoms, strength, tendon reflexes and vibratory sense (range 0-12; PNP >3 points). Kaplan-Meier-type curves were calculated. In total, 22 study centers enrolled 121 patients, 92 assessable for analysis. The probability to exceed a PNP score of 3 increased from 0.20 versus 0.30 after six to 0.68 versus 0.47 after 12 administrations (1 versus 3 h: p = 0.66). After 12 weeks of therapy only a quarter of assessable patients were free of PNP. Cox analysis yielded a relative risk of 1.10 for 1-h infusions (p = 0.80). We observed a rapid increasing risk of PNP manifestation in the course of weekly PAC administrations without significant differences between 1- and 3-h infusions. This is in contrast to pharmacokinetic observations indicating that a shortening of infusion time might enhance neurotoxicity by increasing the AUC of Cremophor. A majority of patients experiencing neurotoxic effects require the investigation of potential nerve protectors in future clinical trials accompanying PAC therapy.

Adolescent↗
PubMed1991

Observer variation in assessing neurophysical signs among patients with head injuries.

As an early phase in the development of a valid and reliable measure of the neurophysical sequelae after head injury, we carried out assessments of interrater agreement on representative items. The purpose of this study was to determine the degree of agreement among expert raters who independently measured neurophysical signs on patients undergoing physical rehabilitation after brain injury. Agreement was described using the index of crude agreement, expected agreement and Kappa. Therapists showed a high degree of agreement on those items forming part of a routine neurological assessment: prehension, coordination, voluntary movements and tendon reflexes. Crude agreement ranged from 77.8-100%. There was considerable discordance in assessing muscle tonus, equilibrium and protective reactions, spinal reflexes, tremor and dysmetria (crude agreement ranged from 49.7-97.9%). Although, the number of subjects was small, the information generated from this study will be useful in refining our instrument for the assessment of neurophysical signs.

Adult↗