Primary bone tumours, even in very advanced stages, rarely exhibit transarticular spread. We present a case of chondrosarcoma of the ilium with destruction of the sacroiliac joint, the ipsilateral sacral ala and with sacral nerve involvement.
A system for assessing the results of tibialis posterior tendon transfers in the treatment of foot drop secondary to nerve palsy is proposed. There are seven sections to this scoring system: pain, need for orthosis, ability to wear normal shoes, activity level, muscle power of ankle dorsiflexion, degree of active ankle dorsiflexion, and foot posture. The total score is 100. The results are classified as excellent for scores between 85 and 100, good between 70 and 84, fair between 55 and 69, and poor for scores below 55. The results of 18 patients (mean followup, 64.6 months) who had a tibialis posterior tendon transfer were assessed using this method. Four patients (22.2%) had an excellent result, seven (38.8%) had a good result, two (11.1%) had a fair result, and five (27.7%) had a poor result. The average score was 67.2, suggesting an overall fair result for this operation. In nine patients, there was correlation between the outcome when assessed with this method and with patient rating. In two patients, the outcomes were better when assessed with this method than with patient rating, whereas the reverse was true in seven other patients. Thus, this system may provide a more objective and critical evaluation of tibialis posterior transfers for foot drop.
Background: Primary palmar hyperhidrosis is a functionally and socially disabling condition. The choice of treatment is controversial.
Objective: To examine the clinical presentation of primary palmar hyperhidrosis and the results of treatment with thoracoscopic sympathectomy in a local setting.
Materials and Methods: A retrospective study of 7 patients involving 10 sympathectomies between October 1997 and October 2000 was undertaken.
Results: The duration of anaesthesia ranged from 55 to 130 minutes with the majority being 1 hour. The immediate results were good, with all operated limbs dry soon after operation. There was no mortality or serious morbidity in this study. All were satisfied with the results of surgery.
Conclusions: Primary palmar hyperhidrosis is not uncommon but rather underdiagnosed. Thoracoscopic sympathectomy is an effective treatment with minimal complications.
Clinical presentation of Menière's disease in children is not as typical as in adults. The triad of vertigo, tinnitus and deafness are not usually elicited, diagnosis often being made after years of follow up and batteries of investigation. A case of Menière's disease in a 3-year-old boy is presented. The diagnosis was only obvious at the age of 8 when the triad of vertigo, deafness and tinnitus were present. His disease progressed despite a trial of intratympanic gentamicin injections and endolymphatic sac decompression. Vestibular nerve section was subsequently performed for his intractable disease. Following the procedure he was asymptomatic and able to attend school.
We report a rare case of left axillary artery injury associated with anterior dislocation of the left shoulder in a 25 yrs old male as a result of a road traffic accident. The shoulder dislocation was reduced. A left upper limb angiogram showed an obstructed left axillary artery. The obstructed segment was surgically reconstructed with a Dacron graft. Six months post operation in follow up, he was found to have good left shoulder function and no neurovascular deficit. This is an injury that could have been easily missed without a simple clinical examination.
Magnetic resonance imaging is gaining importance in the diagnosis of nerve and muscular disorders. The ability of magnetic resonance imaging to delineate the different muscles and the nerve in any plane has made the differentiation between the changes of neuropathy, denervation, and nerve entrapment possible. Although findings on magnetic resonance imaging are non-specific, their use, coupled with clinical symptoms and electromyographic findings, allow an accurate diagnosis to be made without resorting to invasive biopsies.
1 Candoxin (MW 7334.6), a novel toxin isolated from the venom of the Malayan krait Bungarus candidus, belongs to the poorly characterized subfamily of nonconventional three-finger toxins present in Elapid venoms. The current study details the pharmacological effects of candoxin at the neuromuscular junction. 2 Candoxin produces a novel pattern of neuromuscular blockade in isolated nerve-muscle preparations and the tibialis anterior muscle of anaesthetized rats. In contrast to the virtually irreversible postsynaptic neuromuscular blockade produced by curaremimetic alpha-neurotoxins, the neuromuscular blockade produced by candoxin was rapidly and completely reversed by washing or by the addition of the anticholinesterase neostigmine. 3 Candoxin also produced significant train-of-four fade during the onset of and recovery from neuromuscular blockade, both, in vitro and in vivo. The fade phenomenon has been attributed to a blockade of putative presynaptic nicotinic acetylcholine receptors (nAChRs) that mediate a positive feedback mechanism and maintain adequate transmitter release during rapid repetitive stimulation. In this respect, candoxin closely resembles the neuromuscular blocking effects of d-tubocurarine, and differs markedly from curaremimetic alpha-neurotoxins that produce little or no fade. 4 Electrophysiological experiments confirmed that candoxin produced a readily reversible blockade (IC(50) approximately 10 nM) of oocyte-expressed muscle (alphabetagammadelta) nAChRs. Like alpha-conotoxin MI, well known for its preferential binding to the alpha/delta interface of the muscle (alphabetagammadelta) nAChR, candoxin also demonstrated a biphasic concentration-response inhibition curve with a high- (IC(50) approximately 2.2 nM) and a low- (IC(50) approximately 98 nM) affinity component, suggesting that it may exhibit differential affinities for the two binding sites on the muscle (alphabetagammadelta) receptor. In contrast, curaremimetic alpha-neurotoxins have been reported to antagonize both binding sites with equal affinity.
1. Diabetes and hypertension are both associated with an increased risk of renal disease and are associated with neuropathies, which can cause defective autonomic control of major organs including the kidney. This study aimed to examine the alpha(1)-adrenoceptor subtype(s) involved in mediating adrenergically induced renal vasoconstriction in a rat model of diabetes and hypertension. 2. Male spontaneously hypertensive rats (SHR), 220-280 g, were anaesthetized with sodium pentobarbitone 7-day poststreptozotocin (55 mg x kg(-1) i.p.) treatment. The reductions in renal blood flow (RBF) induced by increasing frequencies of electrical renal nerve stimulation (RNS), close intrarenal bolus doses of noradrenaline (NA), phenylephrine (PE) or methoxamine were determined before and after administration of nitrendipine (Nit), 5-methylurapidil (5-MeU), chloroethylclonidine (CEC) and BMY 7378. 3. In the nondiabetic SHR group, mean arterial pressure (MAP) was 146+/-6 mmHg, RBF was 28.0+/-1.4 ml x min(-1) x kg(-1) and blood glucose was 112.3+/-4.7 mg x dl(-1), and in the diabetic SHR Group, MAP was 144+/-3 mmHg, RBF 26.9+/-1.3 ml(-1) min x kg(-1) and blood glucose 316.2+/-10.5 mg x dl(-1). Nit, 5-MeU and BMY 7378 blunted all the adrenergically induced renal vasoconstrictor responses in SHR and diabetic SHR by 25-35% (all P<0.05), but in diabetic rats the responses induced by RNS and NA treated with 5-MeU were not changed. By contrast, during the administration of CEC, vasoconstrictor responses to all agonists were enhanced by 20-25% (all P<0.05) in both the SHR and diabetic SHR. 4. These findings suggest that alpha(1A) and alpha(1D)-adrenoceptor subtypes contribute in mediating the adrenergically induced constriction of the renal vasculature in both the SHR and diabetic SHR. There was also an indication of a greater contribution of presynaptic adrenoceptors, that is, alpha(1B)-, and/or alpha(2)-subtypes.
An earlier study showed that des-aspartate-angiotensin I (DAA-I) attenuated the pressor action of angiotensin III in aortic rings of the spontaneously hypertensive rat (SHR) but not the normotensive Wistar Kyoto (WKY) rat. The present study investigated similar properties of DAA-I in isolated perfused kidneys and mesenteric beds of WKY and SHR. In the renal vasculature, angiotensin III induced a dose-dependent pressor response, which was more marked in the SHR than WKY in terms of significant greater magnitude of response and lower threshold. DAA-I attenuated the pressor action of angiotensin III in both the WKY and SHR. The attenuation in SHR was much more marked, occurring at doses as low as 10(-15) M DAA-I, while effective attenuation was only seen with 10(-9) M in WKY. The effects of DAA-I was not inhibited by PD123319 and indomethacin, indicating that its action was not mediated by angiotensin AT2 receptors and prostaglandins. However, the direct pressor action of angiotensin III in the SHR but not the WKY was attenuated by indomethacin suggesting that this notable difference could be due to known decreased response of renal vasculature to vasodilator prostaglandins in the SHR. Pressor responses to angiotensin III in the mesenteric vascular bed was also dose dependent, but smaller in magnitude compared to the renal response. The responses in the SHR, though generally smaller, were not significantly different from those of the WKY. This trend is in line with the similar observations with angiotensin III and II by other investigators. In terms of the effect of DAA-I, indomethacin and PD123319 on angiotensin III action, similar patterns to those of the renal vasculature were observed. This reaffirms that in the perfused kidney and mesenteric bed, where the majority of the vessels are contractile, femtomolar concentrations of DAA-I attenuates the pressor action of angiotensin III. The attenuation is not indomethacin sensitive and does not involve the angiotensin AT2 receptor. The findings suggest that DAA-I possesses protective vascular actions and is involved in the pathophysiology of hypertension.
Functional dyspepsia (FD) is a common disorder of yet uncertain etiology. Dyspeptic symptoms are usually meal related and suggest an association to gastrointestinal (GI) sensorimotor dysfunction. Cholecystokinin (CCK) is an established brain-gut peptide that plays an important regulatory role in gastrointestinal function. It inhibits gastric motility and emptying via a capsaicin sensitive vagal pathway. The effects on emptying are via its action on the proximal stomach and pylorus. CCK is also involved in the regulation of food intake. It is released in the gut in response to a meal and acts via vagal afferents to induce satiety. Furthermore CCK has also been shown to be involved in the pathogenesis of panic disorder, anxiety and pain. Other neurotransmitters such as serotonin and noradrenaline may be implicated with CCK in the coordination of GI activity. In addition, intravenous administration of CCK has been observed to reproduce the symptoms in FD and this effect can be blocked both by atropine and loxiglumide (CCK-A antagonist). It is possible that an altered response to CCK may be responsible for the commonly observed gastric sensorimotor dysfunction, which may then be associated with the genesis of dyspeptic symptoms.
Dyspepsia itself is not a diagnosis but stands for a constellation of symptoms referable to the upper gastrointestinal tract. It consists of a variable combination of symptoms including abdominal pain or discomfort, postprandial fullness, abdominal bloating, early satiety, nausea, vomiting, heartburn and acid regurgitation. Patients with heartburn and acid regurgitation invariably have gastroesophageal reflux disease and should be distinguished from those with dyspepsia. There is a substantial group of patients who do not have a definite structural or biochemical cause for their symptoms and are considered to be suffering from functional dyspepsia (FD). Gastrointestinal motor abnormalities, altered visceral sensation, dysfunctional central nervous system-enteral nervous system (CNS-ENS) integration and psychosocial factors have all being identified as important pathophysiological correlates. It can be considered as a biopsychosocial disorder with dysregulation of the brain-gut axis being central in origin of disease. FD can be categorized into different subgroups based on the predominant single symptom identified by the patient. This subgroup classification can assist us in deciding the appropriate symptomatic treatment for the patient.
Acute Guillain-Barre syndrome (GBS) is characterized by an acute onset of limb weakness and areflexia. There are a few rare variants that have been described and one of them is the pharyngeal-cervical-brachial (PCB) variant (oropharynx, neck, and proximal upper limb muscles). However, in this patient, the only presentation was bulbar involvement with fast recovery within days. This is likely to be the milder form of PCB that has rarely been described before. A 19-year-old Malay lady presented with progressive dysphagia associated with nasal voice for one week duration. There was no limb weakness. Examination showed generalized areflexia. Pharyngeal and palatal muscles were markedly weak. Cerebrospinal fluid (CSF) examination showed raised protein level. Nerve conduction studies revealed generalized demyelinating motor polyneuropathy consistent with GBS. The patient fully recovered within three days and was discharged well.
This study is designed to evaluate twenty patients after sural nerve harvest using the single longitudinal incision method. The area of sensory loss to pin prick was assessed by the authors at different intervals. Donor site factors, scar cosmesis, functional status and complications were assessed using a questionnaire. The mean area of anaesthesia at one month was 65 cm2 and it had reduced by 77% to 15 cm2 at one and a half years. The mean area of reduced sensation was 49 cm2 at one month and it increased by 18% to 58 cm2 over the same period. Therefore, the total area of sensory deficit was reduced by 36% from 114 cm2 at one month to 73 cm2 at one and a half years. Subjective patient evaluation indicated moderate level of pain during immediate post surgical period, which reduced significantly at one month. A low level of neuroma symptoms was recorded throughout the study period. At a mean follow-up period of two years, there was no area of anaesthesia in 50% of the patients. Mean area of anaesthesia for all patients was 12 cm2 and mean area of reduced sensation was 55 cm2. Subjective patient evaluation indicated a low level of pain, neuroma symptoms and numbness over the sural nerve sensory distribution. Twenty five percent of the patients were not satisfied with the scar appearance. Function and daily activities were not affected significantly. No surgical complications were observed.
Sensorineural hearing loss (SNHL) due to internal auditory canal (IAC) stenosis with hypoplasia of the cochleovestibular nerve is a rare disorder. The diagnosis of the IAC stenosis requires both high resolution computed tomography scan (HRCT) and magnetic resonance imaging (MRI).
The spinal nucleus of the accessory nerve (SNA) comprises the group of somata (perikarya) of motor neurons that supply the sternocleidomastoid and trapezius muscles. There are many conflicting views regarding the longitudinal extent and topography of the SNA, even in the same species, and these disagreements prompted the present investigation. Thirty Sprague-Dawley rats (15 males, 15 females) were used. The SNA was localized by retrograde axonal transport of horseradish peroxidase. Longitudinally, the SNA was found to be located in the caudal part (caudal 0.9-1.2 mm) of the medulla oblongata, the whole lengths of cervical spinal cord segments C1, C2, C3, C4, C5 and rostral fourth of C6. In the caudal part of the medulla oblongata, the SNA was represented by a group of perikarya of motor neurons lying immediately ventrolateral to the pyramidal fibres that were passing dorsolaterally after their decussation. In the spinal cord, the motor neuronal somata of the SNA were located in the dorsomedial and central columns at C1, in the dorsomedial, central and ventrolateral columns at C2 and in the ventrolateral column only at C3, C4, C5 and rostral quarter of C6. The perikarya of motor neurons supplying the sternocleidomastoid were located in the caudal part (caudal 0.9-1.2 mm) of the medulla oblongata ventrolateral to the pyramidal fibres that were passing dorsolaterally after their decussation. They were also located in the dorsomedial and central columns at C1, in the dorsomedial, central and ventrolateral columns at C2 and only in the ventrolateral column at the rostral three-quarters of C3. The perikarya of motor neurons supplying the trapezius muscle were located in the ventrolateral column only in the caudal three-quarters of C2, the whole lengths of C3, C4 and C5, and in the rostral quarter of C6.
This study investigated whether the alpha(1)-adrenoceptor subtype(s) mediating the vasoconstrictor actions of the renal sympathetic nerves were altered in rats with cisplatin-induced renal failure. Male Wistar Kyoto rats were used and half received cisplatin (5 mg/kg i.p.) to induce renal failure and were taken for study 7 days later. The renal blood flow reductions caused by electrical renal nerve stimulation and close intra-renal administration of noradrenaline, phenylephrine and methoxamine were determined before and after amlodopine (AMP), 5-methylurapidil (MeU), chloroethylclonidine (CEC) or BMY 7378. Water intake and creatinine clearance were decreased (P<0.05) by 40-50% while fractional excretion of sodium was increased two-fold in the cisplatin treated rats. Mean arterial pressure was higher, 110+/-2 versus 102+/-3 mmHg and renal blood flow was lower, 10.7+/-0.9 versus 18.9+/-0.1 ml/min/kg in the renal failure rats (both P<0.05). AMP, MeU and BMY 7378 decreased (all P<0.05) the adrenergically induced renal vasoconstrictor responses in the renal failure groups by 30 to 50% and in normal rats by 20 to 40%. In the presence of CEC, renal nerve stimulation and noradrenaline and methoxamine induced renal vasoconstrictor responses were enhanced (all P<0.05) in the renal failure but not in the normal rats. These data showed that alpha(1A)- and alpha(1D)-adrenoceptors were the major subtypes in mediating adrenergically induced renal vasoconstriction but there was no substantial shift in subtype in renal failure. The contribution of alpha(1B)-adrenoceptor subtypes either pre- or post-synaptic appeared to be raised in the renal failure rats.
Botulinum toxin is effective in reducing spasticity post stroke. As there are limited data on post stroke spasticity in Asia, we undertake this study to determine the effectiveness and safety of intramuscular injection of botulinum toxin type-A (BTX-A), in the treatment of chronic focal post-stroke hand spasticity, and the impact of BTX-A on the activities of daily living and quality of life, in comparison to placebo, in Malaysian stroke patients. This was a randomized, double-blind, placebo-controlled study to assess the efficacy and safety of BTX-A in 27 subjects with wrist and finger spasticity after a stroke. The outcome measures were assessed with the Modified Ashworth Scale (MAS) to assess spasticity of the flexor muscles, Barthel Index (BI) for activities of daily living and EQ-5D and EQ VAS for quality of life. Assessments were performed at baseline and 1 and 3 months after injection. Compared to placebo, the BTX-A group had greater improvement in the flexor tone of the wrist and fingers (p = 0.001 and p < 0.001, respectively), at first month follow-up visit and sustained the improvement through to three months. Although there was an improvement in the measures of global function and quality of life in the BTX-A group, there was no significant improvement in between the two groups. No serious BTX-A related adverse effects were reported. The results of this study demonstrate that intramuscular injection of botulinum toxin A is safe and effective in the treatment of chronic focal post-stroke spasticity of the hand.
The pathogenesis of cisplatin-induced renal failure is related to reduced renal blood flow due to severe tubular damage and enhanced renovascular resistance. It is also known that alpha(1)-adrenoceptors, the major subtype of alpha-adrenoceptors in renal vasculature play the pivotal role in regulating renal hemodynamics. With this background, we have hypothesized that the altered renal hemodynamics and enhanced renovascular resistance in cisplatin-induced renal failure might be caused by the altered alpha-adrenergic responsiveness with a possible involvement of alpha(1)-adrenoceptors in the renal vasculature. In a unique experimental approach with anesthetized rats, this study has therefore examined if there is any shift in the renovascular responsiveness to renal nerve stimulation and a series of alpha-adrenergic agonists in Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats with cisplatin-induced renal failure in comparison with their body weight-matched normal controls. Thirty-two male rats of both WKY (n=16) and SHR (n=16) origin with body weight 236+/-7.9 g received cisplatin (5mg/kg i.p.). The renal failure was confirmed in terms of significantly reduced renal blood flow, reduced creatinine clearance, increased fractional excretion of sodium, increased kidney index (all P<0.05) and tubular damage. After 7 days of cisplatin, the overnight fasted rats were anesthetized (sodium pentobarbitone, 60 mg/kg i.p.) and renal vasoconstrictor experiments were done. The changes in the vasoconstrictor responses were determined in terms of reductions in renal blood flow caused by electrical renal nerve stimulation or intrarenal administration of noradrenaline, phenylephrine and methoxamine. It was observed that in the cisplatin-treated renal failure WKY and SHR rats there were significant (all P<0.05) reductions in the renal blood flow along with significantly (P<0.05) higher renal adrenergic responsiveness as compared with their non-renal failure controls. The data showed that in the renal failure WKY and SHR rats, the altered renal hemodynamics might be caused by an augmented renal adrenergic responsiveness. The results obtained further led us to suggest that the augmented renal adrenergic responsiveness in the cisplatin-induced renal failure rats were possibly mediated by the alpha(1)-adrenoceptors.
1 The present study investigated the effect of streptozotocin-induced diabetes on alpha(1)-adrenoceptor subtypes in rat renal resistance vessels. 2 Studies on renal haemodynamics were carried out 7 days after the last streptozotocin. Changes in renal blood flow were recorded in response to electrical stimulation of the renal nerve (RNS) and a range of adrenergic agonists; noradrenaline (NA), phenylephrine (PE) and methoxamine (MTX), either in the absence or the presence of nitrendipine (Nit), 5-methylurapidil (MEU), chlorethylclonidine (CEC) or BMY 7378. 3 In non-diabetic animals, Nit, MEU and BMY 7378 significantly attenuated renal vasoconstriction induced by adrenergic agonists, while CEC showed a significant accentuation in RNS-induced responses without having a significant effect on responses to adrenergic agonists. In diabetic rats, renal vasoconstriction was also significantly reduced in Nit-, MEU- and BMY 7378-treated groups and CEC potentiated RNS-induced contractions caused a change similar to that observed in non-diabetic rats. BMY 7378 significantly (P < 0.05) attenuated the PE- and MTX-induced vasoconstrictions but did not cause any significant (P > 0.05) alteration in the RNS- and NA-induced responses. 4 The results showed functional co-existence of alpha(1A)- and alpha(1D)-adrenoceptors in the renal vasculature of SD rats irrespective of the presence of diabetes. A possible minor contribution of prejunctional alpha-adrenoceptor subtype has also been suggested in either experimental group, particularly possible functional involvement of alpha(1B)-adrenoceptor subtypes in non-diabetic SD rats.