Supplemental peri-operative intravenous crystalloids for postoperative nausea and vomiting: an abridged Cochrane systematic review.

We conducted a Cochrane systematic review on the effectiveness of supplemental intravenous crystalloid administration in preventing postoperative nausea and vomiting. We included randomised controlled trials of patients undergoing surgery under general anaesthesia and given supplemental peri-operative intravenous crystalloid. Our primary outcomes were the risk of postoperative nausea and the risk of postoperative vomiting. We assessed the risk of bias for each included study and applied the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) framework for the certainty of evidence. We included 41 studies. We found that the intervention probably reduces the overall risk of postoperative nausea, the risk ratio (95%CI) being 0.62 (0.51-0.75) (I2  = 57%, p < 0.00001, 18 studies; 1766 participants; moderate-certainty evidence). It also probably reduces the risk of postoperative nausea within 6 h of surgery, with a risk ratio (95%CI) of 0.67 (0.58 to 0.78) (I2  = 9%, p < 0.00001, 20 studies; 2310 participants; moderate-certainty evidence) and by around 24 h, the risk ratio (95%CI) being 0.47 (0.32-0.69) (I2  = 38%, p = 0.0001, 17 studies; 1682 participants; moderate-certainty evidence). Supplemental intravenous crystalloid probably also reduces the overall risk of postoperative vomiting, with a risk ratio (95%CI) of 0.50 (0.40-0.63) (I2  = 31%, p < 0.00001, 20 studies; 1970 participants; moderate-certainty evidence). The beneficial effect on vomiting was seen both within 6 h and by around 24 h postoperatively.

Kainic acid injections result in degeneration of cochlear nucleus cells innervated by the auditory nerve.

When kainic acid, a putative neurotoxin for neurons with glutamatergic input, is injected into the brainstem, it produces a selective pattern of degeneration in the cochlear nucleus. The rate and extent of degeneration is correlated with the distribution of the primary auditory fibers. This evidence supports the hypothesis that glutamate is the neurotransmitter for primary auditory fibers.

Evidence for a dipeptide porter in the lysosome membrane.

Small neutral dipeptides such as Gly-Gly are known to cross the lysosome membrane rapidly. The mode of dipeptide translocation was studied, using an osmotic-protection method. Results with dipeptide analogues, such as omega-amino aliphatic acids and taurine, indicated that dipeptides do not cross the rat liver lysosome membrane by unassisted diffusion. Using seven pairs of dipeptide stereoisomers, the penetration of the L-isomer was always found to be much more rapid than that of the D-analogue. It is concluded that the lysosome membrane contains a porter that recognizes and transports L-dipeptides.

Corticosteroid-responsive dominantly inherited neuropathy in childhood.

We describe three children with corticosteroid-responsive inflammatory demyelinating polyneuropathy from families with dominantly inherited neuropathy. There were atypical clinical, electrophysiologic, and pathologic characteristics that suggested a coexistent inflammatory demyelinating neuropathy and that should alert the clinician to the possibility of an associated acquired, potentially treatable disorder.

Posterior cervical spinal cord infarction following vertebral artery dissection.

There are only two reported cases of unilateral posterior cervical spinal cord infarction as a result of vertebral artery dissection. We describe the first reported case of bilateral posterior spinal cord infarction caused by vertebral artery dissection.

Ross syndrome plus: beyond horner, Holmes-Adie, and harlequin.

BACKGROUND: Ross syndrome is an uncommon disorder characterized by the triad of segmental anhidrosis, hyporeflexia, and tonic pupils. METHODS: The authors describe the clinical findings of five patients with Ross syndrome and detail the results of their pharmacologic and autonomic testing. RESULTS: In four patients, the classic findings of Ross syndrome were accompanied by Horner's syndrome. Other symptoms of dysautonomia were also common. CONCLUSIONS: These findings suggest that Ross syndrome is a dysautonomic condition of varying expression resulting from a generalized injury to ganglion cells or their projections.

Muscle is electrically inexcitable in acute quadriplegic myopathy.

We directly stimulated muscle in three patients with acute quadriplegic myopathy to determine whether paralyzed muscle in this syndrome is electrically excitable. Two of the patients had been treated with neuromuscular blocking agents and corticosteroids, and one patient had been treated with corticosteroids alone. We found that paralyzed muscle is electrically inexcitable in affected patients. Muscle regained electrical excitability over weeks to months. The recovery of muscle excitability paralleled the clinical recovery of patients, suggesting that paralysis in this syndrome is secondary to electrical inexcitability of muscle membrane.

Chronic inflammatory demyelinating polyneuropathy associated with malignant melanoma.

We report three patients who developed chronic inflammatory demyelinating polyneuropathy (CIDP) in association with malignant melanoma. In two cases, melanoma was discovered during the initial evaluation for neuropathy. Two patients also had vitiligo, an antibody-mediated disorder that may complicate melanoma. Melanoma cells and Schwann cells are both of neuroectodermal cell origin, with shared surface antigens. Shared immunoreactivity may account for the association between melanoma and CIDP, as with vitiligo.

Site of autonomic dysfunction in a patient with Ross' syndrome and postganglionic Horner's syndrome.

Ross' syndrome is a rare peripheral nervous system disorder defined by Adie's tonic pupil, hyporeflexia, and segmental anhidrosis. Injury to postganglionic cholinergic fibers is believed to account for the tonic pupil and sweating disturbance. We report a 47-year-old man found to have Ross' syndrome in combination with a complete postganglionic Horner's syndrome. Pharmacologic and sudomotor tests in this unique patient provide further evidence that Ross' syndrome results from injury to sympathetic and parasympathetic ganglion cells or to their postganglionic projections.

Autosomal dominant transmission of Dejerine-Sottas disease (HMSN III).

Hereditary motor-sensory neuropathy type III (HMSN III) (Dejerine-Sottas disease) is a severe demyelinating neuropathy that is traditionally considered autosomal recessive. We report a father and daughter diagnosed with HMSN III by clinical, electrophysiologic, and pathologic criteria, thus showing that it may be transmitted in an autosomal dominant fashion in selected families.

Denervation supersensitivity in the cholinergic septo-hippocampal pathway: a microiontophoretic study.

The purpose of this study was to determine whether denervation supersensitivity could be produced in an identified cholinergic pathway in the CNS of the rat. The mechanism for the development of this phenomenon was also explored. Cholinergic denervation of the hippocampus was accomplished by lesions of the medial septum. The response of hippocampal pyramidal cells to microiontophoretic application of acetylcholine (ACh) and carbachol in lesioned and unlesioned animals was determined by extracellular recording. There was a marked increase (6 X) in sensitivity to ACh 2-43 days following lesions. However, there was no increase in sensitivity to carbachol or glutamate. Other workers have shown that septal lesions cause a large decrease in hippocampal acetylcholinesterase (AChE) which is located mainly presynaptically. The absence of increase in sensitivity to carbachol, a cholinomimetic resistant to hydrolysis by AChE, suggests that the postlesion increase in sensitivity to ACh results from a decrease in its inactivation by AChE. A time course for the development of ACh supersensitivity was found to be similar to the time course of AChE loss previosly reported. Experiments using physostigmine, an AChE inhibitor, demonstrated that inhibition of AChE can potentiate the effects of ACh in unlesioned preparations, but not in lesioned preparations. We conclude: (1) denervation supersensitivity to ACh occurs in the septo-hippocampal pathway; and (2) the supersensitivity is probably due to decreased inactivation of ACh by AChE. The results suggest that presynaptic AChE plays a significant role in modulating the neurotransmitter function of ACh in the septo-hippocampal pathway.

Iontophoretic application of opiates to the locus coeruleus.

The vast majority of morphine-sensitive single units in the area examined were localized to the locus coeruleus. This corresponds well with the known distribution of the highest densities of opiate receptor sites in this region of the midbrain. The effect of iontophoretically applied morphine was a marked and prolonged depression of spontaneous activity. Levorphanol, an opiate agonist, produced an effect similar to that of morphine while comparable doses of dextrorphan, it's clinically inactive stereoisomer, did not. Naloxone and levallorphan prevented as well as reversed the depression due to application of agonists. While the units were depressed following the application of opiate agonists, the cells were still excited by the neurotransmitter acetylcholine. We conclude that (1) neuronal sensitivity to opiates has a high positive correlation with autoradiographically determined opiate receptor sites, and (2) this sensitivity to opiates is blocked by opiate antagonists and is stereospecific in nature.

Effects of neuronal activity on kainic acid neurotoxicity in the ventral cochlear nucleus.

Kainic acid was injected into the brain stem of adult guinea pigs, and the animals were either placed in a sound reducing-chamber or stimulated with 90 dB noise. The pattern and rate of kainic acid-induced degeneration in the anteroventral cochlear nucleus (AVCN) of sound-deprived animals was similar to that in animals exposed to ambient noise [2]. The amount of degeneration was greatly increased in animals stimulated with 90 dB noise. Therefore, although decreased activity in primary auditory fibers does not protect neurons in the AVCN from kainate-induced neurotoxicity, increased auditory stimulation augments the effects of kainic acid in the cochlear nucleus.

Of mice and men (and women and children): scientific and ethical implications of animal models.

1. Animal models of human behavior and disease are commonly used and have contributed significantly to progress in understanding the physiological mechanisms of both normal function and disease, and in the development of effective therapies. 2. Little attention has been given, however, to the scientific and ethical implications of choosing a particular animal model. 3. This paper discusses the rationale for the selection of particular animal models that have been chosen to study certain human diseases or behaviors, and provides examples to illustrate how underlying assumptions about methods and about physiological mechanisms and other relevant features of the disease or behavior of interest are embedded in the choice of an animal model. 4. Although these assumptions influence the direction of research, they are rarely analyzed explicitly, or evaluated empirically. The authors recommend that assumptions should be clearly stated and that, whenever possible, they be specifically and thoroughly evaluated empirically.

Bulbocavernosus reflex studies and autonomic testing in the diagnosis of erectile dysfunction.

The electrophysiologic evaluation of patients with erectile dysfunction presents an important diagnostic challenge. The bulbocavernosus reflex (BCR) latency has been commonly used to evaluate these disorders. However, it is a measure of somatic penile innervation, whereas erection is primarily dependent on autonomic function. We evaluated 195 men with erectile dysfunction over a 3 year period. Each had electrophysiologic studies, nerve conduction studies and a BCR. BCR studies were abnormal in only 7%, of which most had diabetes or pelvic trauma. The BCR was the sole electrophysiologic abnormality in only 2%. Autonomic testing (AT) was additionally performed in 19 diabetic and 23 non-diabetic patients. This included sympathetic skin responses and measurement of the Valsalva ratio and heart rate variability with 6/min breathing. In the diabetic group, AT was positive in 63%, and most often was the sole abnormality. The bulbocavernosus reflex is relatively insensitive in the diagnosis of erectile dysfunction. Brief autonomic testing may provide valuable additional data, particularly in diabetics.

Serial evoked potential studies and MRI imaging in chronic progressive multiple sclerosis.

Measurements of serial evoked potential latencies and plaque burden on MRI scans are often obtained during clinical studies of multiple sclerosis patients to provide additional information to the disability-based primary endpoints. The ideal laboratory-based marker of progression would be expected to significantly change over the time period of study. Serial visual (VEP) and brainstem auditory evoked potentials (BAEP) and MRI scans of 11 chronic progressive MS patients were obtained over a 1.5 year period in a clinical study. Over this period, there was no significant change in disability as measured by the Kurtzke EDSS, Ambulation Index or Neurological Rating Score. The VEP P100 significantly progressed over the period of study. However, the MRI T(2) plaque burden and BAEP I-V intrapeak latency did not significantly progress over the 1.5 years. We conclude that, in chronic progressive MS, serial visual evoked potential tests may complement standard disability-based endpoints to assess disease progression.

Genetic testing for neurologic diseases. A rose with thorns.

Genetic testing for neurologic conditions, including HD, requires that the primary concerns of informed consent, counseling and support, and confidentiality be recognized and addressed. A safe, reliable test should be available to those who want the information and understand the limitations of the testing procedure. However, testing should be in the context of multifaceted counseling, which combines a variety of components. Safeguards for confidentiality should be assured. Predictive testing for hereditary disease emphasizes the need to focus on capabilities rather than disability. This is an extension of the larger reality that continuing advances in health care can extend the length of an individual's life and stave off death without restoring health. Certainly, new developments in molecular biology may provide new tools, but the basic ethical problems are fundamental issues independent of technology. Just as change is not necessarily progress, the application of scientific advances to health care does not automatically benefit humanity. Sensitivity to human needs is the art of applying medical technology.

Prolonged muscle weakness after neuromuscular blockade in the intensive care unit.

As noted, quadriparesis with reduced reflexes and difficulty with ventilator weaning may be seen as a result of a number of neuromuscular disorders. The clinical approach relies on exclusion of a central cause first, followed by careful examination of peripheral nerve and muscle function. Persistent neuromuscular blockade should be excluded initially because it is a readily reversible condition. Use of a train of four stimulation with a peripheral twitch monitor can quickly establish integrity of conduction across the neuromuscular junction. If necessary, further electrophysiologic studies allow differentiation among the relevant diagnostic possibilities. CIP is characterized by nerve conduction and EMG findings consistent with axonal degeneration of sensory and motor fibers. GBS is distinguished by evidence of demyelination on nerve conduction studies, in addition to elevated spinal fluid protein. Persistent neuromuscular blockade is identified by a decremental response on repetitive stimulation studies of neuromuscular transmission. The acute myopathy following neuromuscular blockage does not involve sensory responses. Needle EMG examination reflects a myopathic pattern, rather than a neurogenic one as seen in CIP or GBS. In myopathic patients who are unable to move their limbs at all (precluding a full EMG examination), a muscle biopsy identifies muscle as the site of involvement.