We have before us a patient with neuropathic pain, which due to the origin of the tumor, is most likely due to involvement of the celiac plexus. It is important to have a radiological diagnosis in view of a possible local treatment, such as neurolytic treatment or plexus blockade. However, we should not leave the patient without a treatment that can alleviate but rather solve the current situation. He is taking WHO step 3 analgesia, which is clearly insufficient, so he will need adjuvants; although opioids for neuropathic pain are not very effective, we will not reduce the dose but will associate the adjuvants. We would manage the patient with gabapentin and corticosteroids (true answer 4); we would not decrease the dose of morphine (false answer 3), and in the meantime we would ask for a CT scan (or abdominal MRI) to subsequently assess the plexus block (answers 1 and 2 for future management).

We have before us a patient with neuropathic pain, which due to the origin of the tumor, is most likely due to involvement of the celiac plexus. It is important to have a radiological diagnosis in view of a possible local treatment, such as neurolytic treatment or plexus blockade. However, we should not leave the patient without a treatment that can alleviate but rather solve the current situation. He is taking WHO step 3 analgesia, which is clearly insufficient, so he will need adjuvants; although opioids for neuropathic pain are not very effective, we will not reduce the dose but will associate the adjuvants. We would manage the patient with gabapentin and corticosteroids ([HIDDEN]); we would not decrease the dose of morphine ([HIDDEN]), and in the meantime we would ask for a CT scan (or abdominal MRI) to subsequently assess the plexus block ([HIDDEN]).

A 66-year-old patient diagnosed with stage IV pancreatic adenocarcinoma 8 months ago. He follows treatment with delayed release morphine 200 mg/12 hours orally, kerosene and lactulose. For the last 15 days he has reported paresthesias and occasional lancinating pain in the right lumbar and periumbilical area that does not subside with rescue morphine. The neurological examination is normal. Indicate the most appropriate management:

Perform computed axial tomography and evaluate nerve compression since it is neuropathic pain.

Evaluate neurolytic treatment since neuropathic pain is difficult to control.

Decrease the dose of morphine as it is ineffective in this type of pain.

Administer amitriptyline or gabapentin, dexamethasone and increase the dose of morphine.

Neuralgia

Treatment Treatment options include medicines and surgery. Neuralgia is more difficult to treat than other types of pain because it does not respond well to normal pain medications. Special medications have become more specific to neuralgia and typically fall under the category of membrane stabilizing drugs or antidepressants such as Cymbalta. The antiepileptic medication(AED) Lyrica (pregabalin) was developed specifically for neuralgia and other neuropathic pain as a successor to Neurontin (gabapentin). High doses of anticonvulsant medicines—used to block nerve firing— and tricyclic antidepressants are generally effective in treating neuralgia. If medication fails to relieve pain or produces intolerable side effects, surgical treatment may be recommended.

Morphine for chronic neuropathic pain in adults.

Neuropathic pain, which is caused by a lesion or disease affecting the somatosensory system, may be central or peripheral in origin. Neuropathic pain often includes symptoms such as burning or shooting sensations, abnormal sensitivity to normally painless stimuli, or an increased sensitivity to normally painful stimuli. Neuropathic pain is a common symptom in many diseases of the nervous system. Opioid drugs, including morphine, are commonly used to treat neuropathic pain. Most reviews have examined all opioids together. This review sought evidence specifically for morphine; other opioids are considered in separate reviews. To assess the analgesic efficacy and adverse events of morphine for chronic neuropathic pain in adults. We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, and Embase for randomised controlled trials from inception to February 2017. We also searched the reference lists of retrieved studies and reviews, and online clinical trial registries. We included randomised, double-blind trials of two weeks' duration or longer, comparing morphine (any route of administration) with placebo or another active treatment for neuropathic pain, with participant-reported pain assessment. Two review authors independently extracted data and assessed trial quality and potential bias. Primary outcomes were participants with substantial pain relief (at least 50% pain relief over baseline or very much improved on Patient Global Impression of Change scale (PGIC)), or moderate pain relief (at least 30% pain relief over baseline or much or very much improved on PGIC). Where pooled analysis was possible, we used dichotomous data to calculate risk ratio (RR) and number needed to treat for an additional beneficial outcome (NNT) or harmful outcome (NNH). We assessed the quality of the evidence using GRADE and created 'Summary of findings' tables. We identified five randomised, double-blind, cross-over studies with treatment periods of four to seven weeks, involving 236 participants in suitably characterised neuropathic pain; 152 (64%) participants completed all treatment periods. Oral morphine was titrated to maximum daily doses of 90 mg to 180 mg or the maximum tolerated dose, and then maintained for the remainder of the study. Participants had experienced moderate or severe neuropathic pain for at least three months. Included studies involved people with painful diabetic neuropathy, chemotherapy-induced peripheral neuropathy, postherpetic neuralgia criteria, phantom limb or postamputation pain, and lumbar radiculopathy. Exclusions were typically people with other significant comorbidity or pain from other causes.Overall, we judged the studies to be at low risk of bias, but there were concerns over small study size and the imputation method used for participants who withdrew from the studies, both of which could lead to overestimation of treatment benefits and underestimation of harm.There was insufficient or no evidence for the primary outcomes of interest for efficacy or harm. Four studies reported an approximation of moderate pain improvement (any pain-related outcome indicating some improvement) comparing morphine with placebo in different types of neuropathic pain. We pooled these data in an exploratory analysis. Moderate improvement was experienced by 63% (87/138) of participants with morphine and 36% (45/125) with placebo; the risk difference (RD) was 0.27 (95% confidence interval (CI) 0.16 to 0.38, fixed-effects analysis) and the NNT 3.7 (2.6 to 6.5). We assessed the quality of the evidence as very low because of the small number of events; available information did not provide a reliable indication of the likely effect, and the likelihood that the effect will be substantially different was very high. A similar exploratory analysis for substantial pain relief on three studies (177 participants) showed no difference between morphine and placebo.All-cause withdrawals in four studies occurred in 16% (24/152) of participants with morphine and 12% (16/137) with placebo. The RD was 0.04 (-0.04 to 0.12, random-effects analysis). Adverse events were inconsistently reported, more common with morphine than with placebo, and typical of opioids. There were two serious adverse events, one with morphine, and one with a combination of morphine and nortriptyline. No deaths were reported. These outcomes were assessed as very low quality because of the limited number of participants and events. There was insufficient evidence to support or refute the suggestion that morphine has any efficacy in any neuropathic pain condition.

Trigeminal neuralgia

Medical The anticonvulsant carbamazepine is the first line treatment; second line medications include baclofen, lamotrigine, oxcarbazepine, phenytoin, gabapentin and pregabalin. Uncontrolled trials have suggested that clonazepam and lidocaine may be effective. Antidepressant medications, such as amitriptyline have shown good efficacy in treating trigeminal neuralgia, especially if combined with an anti-convulsant drug such as pregabalin. There is some evidence that duloxetine can also be used in some cases of neuropathic pain, especially in patients with major depressive disorder as it is an antidepressant. However, it should, by no means, be considered a first line therapy and should only be tried by specialist advice. There is controversy around opiate use such as morphine and oxycodone for treatment of TN, with varying evidence on its effectiveness for neuropathic pain. Generally, opioids are considered ineffective against TN and thus should not be prescribed.

A comparative efficacy of amitriptyline, gabapentin, and pregabalin in neuropathic cancer pain: a prospective randomized double-blind placebo-controlled study.

Neuropathic pain is difficult to diagnose and difficult to treat with certainty. So the aim of the study was to evaluate comparative clinical efficacy of pregabaline with amitriptyline and gabapentin in neuropathic cancer pain. A total of 120 patients with cancer having severe neuropathic cancer pain were enrolled in the study after taking approval from Institutional Ethics Committee and divided in to 4 groups: group AT-amitriptyline, group GB-gabapentin, group PG-pregabalin, and group PL-placebo. Oral morphine was used for rescue analgesic for continued pain. Pain score (Visual Analogue scale) and secondary outcome measures such as intensity of lancinating, dysesthesia, and burning on numerical rating scale, Global satisfaction score (GSS), Eastern Co-operative Oncology Group scoring (ECOG), and adverse effects were assessed. At the end of study there was significant decrease in pain score in group PG as compared to the other groups; group AT (P = .003), group GB (P = .042), and group PL (P = .024). Percentage of patients with lancinating pain and dysesthesia were significantly less in group PG as compared to groups GB and PL. All the patients in group PL needed rescue morphine. After 4 visits, maximum improvement in ECOG scoring and GSS scoring was observed in group PG patients. Our results suggested that all antineuropathic drugs are effective in relieving cancer-related neuropathic pain. There was statistically and clinically significant morphine sparing effect of pregabaline in relieving neuropathic cancer pain and neuropathic symptoms as compared to other antineuropathic drugs.

[Epidural injection shows no advantages over oral medication and physiotherapy in the treatment of sciatica, irrespective of the duration of symptoms].

The study presented here investigated the short-term effectiveness of one-off lumbar caudal epidural injection (EI) in sciatica in relationship to the reported duration of pain. This retrospective analysis involved 106 consecutive in-patients who received either conservative treatment (Group I) or an additional EI on the first day of their treatment (Group II). Both groups were divided according to the duration of symptoms at the time of admission (less than three months, or more than six months). Propensity score matching was performed for the whole collective and the resulting subgroups. This incorporated gender, age and pain intensity at the time of admission. The target parameter were changes on a visual analogue scale (VAS) of pain intensity on days D1, D3, and D10 depending on the respective treatment. A routine evaluation of the mental variables anxiety, depression and somatisation was performed as part of the examination upon admission and their relationship to the success of treatment was later assessed. The mean age of the patients was 61.7 (± 11.6) in Group I and 63.6 (± 13.6) in Group II. 59 % of the patients were female (n = 63). The Lasègue sign was prevalent in 45 % of Group I and 51 % of Group II. The intensity of pain on the day of admission was similar in both groups (7.0 ± 1.0 for Group I, 6.7 ± 1.8 for Group II). The length of stay on the ward was also similar in both groups (10.2 ± 3.9 and 9.4 ± 3.7 d, respectively). It was found that, independent of the duration of symptoms, injection treatment was significantly more effective than conservative treatment only in the early stages (D1 and D3, p < 0.001). No differences could be found in the expression of these mental variables between treatment groups, as these factors showed no influence on the results of therapy. In the context of acute treatment a once only lumbar caudal epidural injection represents at most a short-term effectiveness for the therapy of sciatica. The results presented here indicate that neither the duration of symptoms nor the measured psychometric variables show any effect on the success of therapy.

Gabapentin as add-on to morphine for severe neuropathic or mixed pain in children from age 3 months to 18 years - evaluation of the safety, pharmacokinetics, and efficacy of a new gabapentin liquid formulation: study protocol for a randomized controlled trial.

Gabapentin has shown efficacy in the treatment of chronic neuropathic or mixed pain in adults. Although pediatric pain specialists have extensive experience with gabapentin for the treatment of neuropathic pain, its use is off-label. Its efficacy and safety in this context have never been shown. The aim of this trial is to compare gabapentin with placebo as add-on to morphine for the treatment of severe chronic mixed or neuropathic pain in children. This trial is part of the European Union Seventh Framework Programme project Gabapentin in Paediatric Pain (GAPP) to develop a pediatric use marketing authorization for a new gabapentin suspension. The GAPP-2 study is a randomized, double-blind, placebo-controlled, multicenter superiority phase II study in children with severe chronic neuropathic or mixed pain. Its primary objective is to evaluate the efficacy of a gabapentin liquid formulation as adjunctive therapy to morphine. Sixty-six eligible children 3 months to 18 years of age with severe pain (pain scores ≥ 7), stratified in three age groups, will be randomized to receive gabapentin (to an accumulating dose of 45 to 63 mg/kg/day, dependent on age) or placebo, both in addition to morphine, for 12 weeks. Randomization will be preceded by a short washout period, and treatment will be initiated by a titration period of 3 weeks. After the treatment period, medication will be tapered during 4 weeks. The primary endpoint is the average pain scores in the two treatment groups (average of two measures each day for 3 days before the end-of-study visit [V10] assessed by age-appropriate pain scales (Face, Legs, Activity, Cry, Consolability scale; Faces Pain Scale-Revised; Numeric Rating Scale). Secondary outcomes include percentage responders to treatment (subjects with 30% reduction in pain scale), number of episodes of breakthrough pain, number of rescue interventions, number of pain-free days, participant dropouts, quality of life (Pediatric Quality of Life Inventory), and acceptability of treatment. Outcomes will be measured at the end-of-study visit after 12 weeks of treatment at the optimal gabapentin dose. Groups will be compared on an intention-to-treat basis. We hope to provide evidence that the combination of morphine and gabapentin will provide better analgesia than morphine alone and will be safe. We also aim to obtain confirmation of the recommended pediatric dose. EudractCT, 2014-004897-40 . Registered on 7 September 2017. ClinicalTrials.gov, NCT03275012 . Registered on 7 September 2017.

[Effectiveness and time to onset of pregabalin in patients with neuropathic pain].

The data from a previously published 12-week randomised, double-blind, placebo-controlled multicentre study on the efficacy and safety of pregabalin were analyzed for time to onset of analgesic action with neuropathic pain. A total of 338 patients with postherpetic neuralgia or painful diabetic peripheral neuropathy were treated with flexible or fixed regimens of pregabalin at daily doses of up to 600 mg/day (n=141 and 132, respectively) or placebo (n=65). Under fixed dose treatment, a decrease of one full point on the 11-point numerical rating pain scale was reached on day 1, two full points on day 13, and three full points on day 23 (under flexible dose pregabalin: on days 6, 17 and 30). In both treatment arms, pain reduction was statistically significant (P=0.001, P=0.002 vs placebo, respectively). In patients with chronic neuropathic pain, the analgesic effect of both pregabalin treatment regimens was high and associated with a rapid time to onset.

Porphyria

Neurologic and psychiatric disorders Patients who experience frequent attacks can develop chronic neuropathic pain in extremities as well as chronic pain in the abdomen. Intestinal pseudo-obstruction, ileus, intussusception, hypoganglionosis, and encopresis in children have been associated with porphyrias. This is thought to be due to axonal nerve deterioration in affected areas of the nervous system and vagal nerve dysfunction. Pain treatment with long-acting opioids, such as morphine, is often indicated, and, in cases where seizure or neuropathy is present, gabapentin is known to improve outcome.

[The influence of dexamethasone on pain after lumbar disc surgery. A double-blind study.].

Patients operated because of lumbar disc herniations (104 patients) were included in a randomized double-blind study analyzing the influence of dexamethasone versus placebo on postoperative drug requirements and the pain score on the visual analogue scale. High doses of dexamethasone had been administered: 40 mg i.v. on the night before the operation; 8 mg intraoperatively topical perineural application; 8 mg i.v. in the evening of the day of operation; 2x8 mg i.m. on days 1 and 2 postoperatively; 2x4 mg i.m. on days 3 and 4; 4 mg po on day 5 and 6 postoperatively. A significant decrease in the requirement for analgesics was found in the drug-treated group, particularly male patients, and also an impressive reduction in the lumbar pain score. In conclusion, there was good alleviation of sciatic pain in the dexamethasone-treated group of females during the 1st week after operation, but we found no evidence that the agent tested had an influence on the clinical outcome 1 month following the operation.

Morphine

Extended-release There are extended-release formulations of orally administered morphine whose effect last longer, which can be given once per day. Brand names for this formulation of morphine include Avinza, Kadian, MS Contin and Dolcontin. For constant pain, the relieving effect of extended-release morphine given once (for Kadian) or twice (for MS Contin) every 24 hours is roughly the same as multiple administrations of immediate release (or "regular") morphine. Extended-release morphine can be administered together with "rescue doses" of immediate-release morphine as needed in case of breakthrough pain, each generally consisting of 5% to 15% of the 24-hour extended-release dosage.

Management of postoperative pain after Lumbar surgery-pregabalin for one day and 14 days-a randomized, triple-blinded, placebo-controlled study.

Despite the progress in understanding acute pain physiology during recent decade, eighty percent of patients still suffer from post-operative discomfort. Pregabalin is an anticonvulsant agent that is approved for painful neuropathies in diabetic patients and post herpetic neuralgia. The main objective of the present study was to compare the improvement in post-operative pain management and patient lifestyle in 3 groups, as first group received placebo, second who received Pregabalin for one day and the last group those who received it for 14 days. This was a prospective single center, randomized, triple-blind, 3-arm, parallel group study. In this triple-blind study, patients were randomized to 1 of 3 groups using computer-generated random number table. 1) The first group received placebo for 14 days, the second group received Pregabalin 300mg 8h preoperatively and 150mg 12 and 24h postoperatively and for the rest of 13days received placebo and the third group received Pregabalin 300mg eight hours preoperatively and 15mg every 12h postoperatively for 14 days. Name, age, gender, height, weight, education, duration of pain, past medical history, drug history,total morphine requirement at the time of discharge and MRI findings of all the patients were recorded, also they Numerical scale system (NRS) and Oswestry low back pain disability index (ODI) questionnaire were completed for them. All the patients were operated based on standard surgery techniques, bilateral foramenotomy and interlaminar discectomy. Of the 105 patients who entered the run-in period, 47 patients (44.8%) were female and 58 (55.2%) were male. The Patients radicular pain mean score based on NRS estimated before surgery was 7.22±1.95 in pregabalin14, 7.71±1.84 in pregabalin1 and 7.45±1.9 in control group. There were no statically significant differences between three groups (P-Value>0.05). The Patients back pain mean score based on NRS was 5.2±2.87 in pregabalin14, 5.11±3.23 in pregabalin1 and 6.4±3.06 in control group. This means that there were no significant differences in the overall score among those three groups (P-Value>0.05). In comparison to their preoperative pain, the average radicular pain in each group of patients improved significantly 4, 8, 12 and 24h after the operation (P-Value<0.001), but there were no significant differences in radicular pain improvements comparing three groups. The results of this study indicate that 1day and 2 weeks post-operative 300mg pregabalin administration may not improve acute pain, morphine consumption and quality of life of patients after surgery. It seems that the diseases cause chronic pain that requires long-term treatment with higher doses.

Tramadol

Its analgesic effects take about one hour to come into effect and 2 to 4 h to peak after oral administration with an immediate-release formulation. On a dose-by-dose basis, tramadol has about one-tenth the potency of morphine (thus 100 mg is commensurate with 10 mg morphine but may vary) and is practically equally potent when compared with pethidine and codeine. For pain moderate in severity, its effectiveness is equivalent to that of codeine at low doses, and hydrocodone at very high doses; for severe pain it is less effective than morphine. These painkilling effects last about 6 h. The potency of analgesia varies considerably as it depends on an individual's genetics. People with specific variants of CYP2D6 enzymes may not produce adequate amounts of the active metabolite (desmetramadol) for effective pain control.

[Treatment of sciatica by lumbar nerve root canal injection under X-ray angiography].

To investigate the short-term clinical effect of lumbar nerve root canal injection under X-ray angiography in the treatment of sciatica. The clincal data of 78 patients with sciatica underwent lumbar nerve root canal injection under X-ray angiography from December 2017 to February 2020 was retrospectively analyzed. Including 31 males and 47 females, aged from 22 to 88 years old with a median of 65 years. There were 55 cases of lumbar disc herniation and 23 cases of lumbar spinal stenosis, the course of disease ranged from 1 to 8 weeks with a median of 3 weeks. There were 71 cases of single segment disc herniation or stenosis, including L<sub3,4</sub of 5 cases, L<sub4,5</sub of 61 cases, L<sub5</subS<sub1</sub of 5 cases, and 7 cases of multisegment herniation or stenosis. The pain visual analogue scale (VAS) was recorded and Macnab was used to evaluate the clinical effect. All patients completed standardized treatment without serious adverse reactions. VAS were (3.21±0.76) scores immediately after treatment, (2.89±0.33) scores 1 hour after treatment, (1.80±0.27) scores 6 hours after treatment, (1.10±0.20) scores 24 hours after treatment, (2.53±0.35) scores 1 week after treatment and (4.27±0.36) scores 1 month after treatment. There were significant differences in VAS between before treatment(7.83±0.56) and each time period after treatment(<iP</i<0.05). According to Macnab low back pain evaluation standard, 42 cases were effective, 34 cases were markedly effective and 2 cases were ineffective within 24 hours after treatment, with an effective rate of 97.4%;38 cases were effective, 25 cases were markedly effective, 15 cases were ineffective within one week after treatment, the effective rate was 80.0%;32 cases were effective, 22 cases were markedly effective, 24 cases were ineffective within one month after treatment, the effective rate was 69.2%. The short-term clinical effect of nerve root canal injection under X-ray radiography in the treatment of sciatica is good and it is an effective method to relieve sciatica.

Amitriptyline in neuropathic cancer pain in patients on morphine therapy: a randomized placebo-controlled, double-blind crossover study.

Amitriptyline is the most common analgesic adjuvant used in cancer patients with neuropathic pain, even though no specific studies have demonstrated a benefit. A randomized placebo-controlled, double-blind crossover study was designed to evidence the effects of amitriptyline in patients with neuropathic cancer pain. Sixteen advanced cancer patients with neuropathic pain on systemic morphine therapy, no longer receiving oncologic treatment, presenting moderate pain (about 4 or more, but less than 7, on a numerical scale of 0-10) in the last week, and given a stable morphine dose in the last 2 days were admitted to the study. During the first week of study, patients were administered 25 mg of amitriptyline or equivalent drops of placebo at night for 3 days and 50 mg for the following 4 days. Doses for patients aged more than 65 years were 15 mg (first 3 days) and 30 mg (3 days after). After a week, a crossover took place for the second week, with the other treatment at an inverse sequence. Opioid consumption, pain intensity, symptoms and adverse effects, mood, sleep, patient's preference, quality of life before starting the study, the first week after and the second week after were recorded. No significant benefits in analgesia were found in the global pain intensity of the previous week of treatment, the least pain intensity or the pain evaluated just after a week of treatment, at the moment of the visit, when amitriptyline was compared with placebo. A significant difference was evidenced for the worst pain (P < 0.035). No differences in opioid doses during the period of study were found. Drowsiness, confusion and dry mouth were significantly more intense with amitriptyline than with placebo (P < 0.036, 0.003, and 0.034, respectively). There were no substantial differences between the two treatments in Spitzer's quality of life score and for each item. No differences in patients' preference for the two treatment periods were found. The analgesic effects of amitriptyline were slight and associated with adverse effects. In light of the results obtained in the study, the extensive use of the drug for cancer pain should be questioned.

[Pharmacological treatment of neuropathic pain].

Neuropathic pain (NP), in view of its non-nociceptive component, is not caused by physiological lesions but by problems in the nervous system itself, whether in the central nervous system (CNS) or peripheral nervous system (PNS). This particular action mechanism makes NP a very difficult-to-treat condition, resistant to most of the commonly used analgesic drugs. A recent study stated that NP has an incidence of 1.24% over the general population, and this percentage increases if we consider acute radiculopathies and some recurrent neuropathies, frequently considered not only neuropathic pain but also nociceptive. Thus, the improvement of NP treatment has become a public health necessity. While WHO recommendations include a three-lined scale in pain treatment -including NSAIDs as the first-line drugs, soft opioids (tramadol or codein) as the second-line, and strong opioids (morphine, oxycodone, and phentanyl) as the third-line- some studies have found this rationale not useful in NP treatment. Based on several studies as STEP, Spanish Pain Society recommendations included antidepressant and anticonvulsant drugs as the first line treatment. Pregabalin, a new neuromodulators class drug, provides a pharmacokinetic profile than its predecessors (phenytoin, carbamazepine, gabapentin, topiramate, oxcarbazepine, and lamotrigine), and showed effectiveness controlling peripheral neuropathic pain. Thus, pregabalin opened the door to a new approach to NP. Other pain societies, such as the Canada Pain Society, have also included pregabalin in the first line treatment of NP. In fact, gabapentin and pregabalin are the current standard care in most of NP-associated diseases.

Extended-release morphine

Dosage comparison For constant pain, the relieving effect of extended-release morphine given once (for Kadian) or twice (for MS Contin) every 24 hours is roughly the same as multiple administrations of immediate release (or "regular") morphine. Morphine sulfate pentahydrade (trade names including Dolcontin) has a higher molecular mass than morphine base, and therefore 10 mg morphine sulfate pentahydrate contains approximatively 7.5 mg of morphine free base. Extended-release morphine can be administered together with "rescue doses" of immediate-release morphine pro re nata in case of breakthrough pain, each generally consisting of 5% to 15% of the 24-hour extended-release dosage.

Efficacy and Safety of Lidocaine Infusion Treatment for Neuropathic Pain: A Randomized, Double-Blind, and Placebo-Controlled Study.

Lidocaine infusion therapy (LIT) is an effective treatment for relieving neuropathic pain (NeP). However, it remains unclear whether pain relief can be sustained through repeated lidocaine infusions. This study aimed to determine whether repeated intravenous administration of low-dose lidocaine could provide prolonged pain relief in patients with specific NeP conditions. This is a prospective, randomized, double-blind, placebo-controlled, parallel study. We compared the efficacy and safety of lidocaine infusions (3 mg/kg) in the LIT group and normal saline infusions in the control group once a week for 4 consecutive weeks in patients with postherpetic neuralgia or complex regional pain syndrome type II. The primary outcome was the difference in the percentage change in the 11-point numerical rating scale (NRS) pain score from baseline to after the final infusion. Secondary outcomes included pain scores during 4 weeks of follow-up and any complications. Forty-two patients completed this study protocol. The percentage reduction in NRS pain scores after the final infusion was significantly greater in the LIT group compared with the control group (P = 0.011). However, this pain reduction was not detectable at the 4-week follow-up. The difference in the percentage change in NRS pain scores was especially prominent in the LIT group after the third and fourth infusions. None of the study participants experienced serious complications from the treatment. Lidocaine infusion therapy (3 mg/kg of lidocaine administered over 1 hour) provided effective short-term pain relief, which was substantially prominent after repeated infusions were administered to patients with refractory NeP. This study was registered at ClinicalTrials.gov, identifier NCT02597257.

[Non-steroidal anti-inflammatory agents. Evaluation criteria in discal sciatic neuralgia].

Few controlled trials have been carried out with non-steroidal antiinflammatory drugs in this indication, mainly as a result of methodological difficulties. A prerequisite for correct evaluation is compliance with certain fundamental principles. The study must be controlled (i.e. comparative, prospective randomized, double-blind, with data quality control and statistical analysis). The sample size must be consistent with the objectives (at least 40 patients per group). The selection criteria must be well specified and the comparability of baseline data assessed. The most appropriate study design for assessing clinical efficacy is to compare two parallel groups of out patients treated during five to fifteen days. The main criterion of efficacy should be based on the judgments of both patients and physician. Time course of pain, improvement in the patient's functional capacity, improvement in physical findings (Schober, Lasègue), dosage of concomitant analgesic treatments when these are allowed, and evaluation at three and six months can also be used as efficacy criteria. Assessment of clinical and biological tolerance is mandatory. Considering the frequent use of non-steroidal antiinflammatory drugs in treating sciatica, there is a strong need for rigorous investigations.

A combination of gabapentin and morphine mediates enhanced inhibitory effects on dorsal horn neuronal responses in a rat model of neuropathy.

Peripheral nerve damage can result in severe, long-lasting pain accompanied by sensory deficits. This neuropathic pain remains a clinical problem, and effective morphine analgesia is often limited by intolerable side effects. The antiepileptic gabapentin has recently emerged as an alternative chronic pain treatment. Improved management of the diverse symptoms and mechanisms of neuropathic pain may arise from combination therapy, based on multiple pharmacologic targets and low drug doses. The authors used the Kim and Chung rodent model of neuropathy to induce mechanical and cold allodynia in the ipsilateral hind paw. In vivo electrophysiologic techniques were subsequently used to record evoked dorsal horn neuronal responses in which the effects of systemic morphine and gabapentin were investigated, both individually and in combination. Morphine (1 and 4 mg/kg) inhibited neuronal responses of control rats but not after neuropathy. Gabapentin (10 and 20 mg/kg) inhibited neuronal responses in nerve injured rats and to a lesser extent in sham rats but not in naive rats. In the presence of gabapentin (ineffective low dose of 10 mg/kg), morphine (1 and 3 mg/kg) mediated significant inhibitory effects in all experimental groups, with the greatest inhibitions observed in spinal nerve-ligated and sham-operated rats. After neuropathy, inhibitions mediated by morphine were significantly increased in the presence of gabapentin compared with morphine alone. After spinal nerve ligation, the inhibitory effects of systemic morphine on evoked dorsal horn neuronal responses are reduced compared with control, whereas the effectiveness of systemic gabapentin is enhanced. In combination with low-dose gabapentin, significant improvement in the effectiveness of morphine is observed, which demonstrates a clinical potential for the use of morphine and gabapentin combinational treatment for neuropathic pain.

Neurology_Adams

Several types of spinal injections, including epidural, root, and facet blocks, have long been used for the treatment of spinal pain. Injections of epidural corticosteroids or mixtures of analgesics and steroids have been helpful in selected cases of lumbar or thoracic nerve root pain, and occasionally in painful peripheral neuropathy, but precise criteria for the use of this measure are not established. Several randomized trials have failed to support a long term beneficial effect of these treatments but a number of our patients have been helped, if only for several days or weeks (see Chap. 10 for a more complete discussion of these approaches). Nerve root blocks with lidocaine or with longer-acting local anesthetics are sometimes helpful in establishing the precise source of radicular pain. Their main therapeutic use in our experience has been for thoracic radiculitis from shingles, chest wall pain after thoracotomy, and diabetic radiculopathy. Similar local injections are used in

Active placebo

An active placebo is a placebo that produces noticeable side effects that may convince the person being treated that they are receiving a legitimate treatment, rather than an ineffective placebo. Nomenclature According to a 1965 paper, the term "concealed placebo" (German: Kaschiertes Placebo) was suggested in a 1959 paper published in German. Example An example of an active placebo is the 1964 work of Shader and colleagues who used a combination of low-dose phenobarbital plus atropine to mimic the sedation and dry mouth produced by phenothiazines. Morphine and gabapentin are painkillers with the common side effects of sleepiness and dizziness. In a 2005 study assessing the effects of these painkillers on neuropathic pain, lorazepam was chosen as an active placebo because it is not a painkiller but it does cause sleepiness and can cause dizziness.

Gabapentin

The oral bioavailability of gabapentin is approximately 80% at 100 mg administered three times daily once every 8 hours, but decreases to 60% at 300 mg, 47% at 400 mg, 34% at 800 mg, 33% at 1,200 mg, and 27% at 1,600 mg, all with the same dosing schedule. Drugs that increase the transit time of gabapentin in the small intestine can increase its oral bioavailability; when gabapentin was co-administered with oral morphine, the oral bioavailability of a 600 mg dose of gabapentin increased by 50%. Gabapentin at a low dose of 100 mg has a Tmax (time to peak levels) of approximately 1.7 hours, while the Tmax increases to 3 to 4 hours at higher doses. Food does not significantly affect the Tmax of gabapentin and increases the Cmax and area-under-curve levels of gabapentin by approximately 10%.

Intra-Venous Lidocaine to Relieve Neuropathic Pain: A Systematic Review and Meta-Analysis.

<bBackground:</b The prevalence of neuropathic pain is estimated to be between 7 and 10% in the general population. The efficacy of intravenous (IV) lidocaine has been studied by numerous clinical trials on patients with neuropathic pain. The aim of this systematic review and meta-analysis was to evaluate the efficacy of IV lidocaine compared with a placebo for neuropathic pain and secondly to assess the safety of its administration. <bMethods:</b A literature search on PubMed, Scopus, CENTRAL (Cochrane Central Register of Controlled Trials), and Google scholar databases was performed for relevant studies published up to February 2019. Randomized controlled trials (RCTs) evaluating IV lidocaine treatment for pain relief in patients with neuropathic pain were included. <bResults:</b 26 articles met the inclusion criteria. Patients with varied etiology of neuropathic pain were among the patient samples of these studies. Fifteen articles were included for quantitative analysis. Lidocaine was superior to a placebo in relieving neuropathic pain in the early post-infusion period [Mean Difference (MD) = -11.9; 95% Confidence interval (CI): -16.8 to -7; <ip</i < 0.00001]. Multiple infusions of lidocaine over a period of 4 weeks, however, had no significant effect on reliving neuropathic pain (MD = -0.96; 95% CI: -2.02 to 0.11; <ip</i = 0.08). IV lidocaine was also associated with a significant number of adverse events compared to a placebo [Odds Ratio (OR) = 7.75; 95% CI: 3.18-18.92; <ip</i < 0.00001]. <bConclusion:</b Our study indicates that while IV lidocaine is effective in pain control among patients with neuropathic pain in the immediate post-infusion period, it does not have a long-lasting, persistent effect. IV infusions of the drug are associated with an increased risk of side effects compared to a placebo. However, the risk of serious adverse events is negligible. Further, well-designed RCTs evaluating the effects of various dosages and infusion periods of IV lidocaine are required to provide clear guidelines on its clinical use.

Morphine

Further studies on the effects of morphine on the immune system have shown that morphine influences the production of neutrophils and other cytokines. Since cytokines are produced as part of the immediate immunological response (inflammation), it has been suggested that they may also influence pain. In this way, cytokines may be a logical target for analgesic development. Recently, one study has used an animal model (hind-paw incision) to observe the effects of morphine administration on the acute immunological response. Following hind-paw incision, pain thresholds and cytokine production were measured. Normally, cytokine production in and around the wounded area increases in order to fight infection and control healing (and, possibly, to control pain), but pre-incisional morphine administration (0.1 mg/kg to 10.0 mg/kg) reduced the number of cytokines found around the wound in a dose-dependent manner. The authors suggest that morphine administration in the acute post-injury period

Microsurgery versus Medical Treatment for Neuropathic Pain Caused by Foraminal Extraforaminal Lumbar Disc Herniation: An Observational Study.

To investigate the incidence of neuropathic pain (NP) in patients with foraminal/extraforaminal lumbar disc herniation (FEFLDH), the prognosis of NP and the effect of microsurgery on patients treatment. Two patient groups with FEFLDH were investigated: the surgery group underwent surgical treatment, and the medical-treated group received medical treatment. Patients were diagnosed with NP when the Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs (S-LANSS) pain scale was ≥ 12 points. The NP scores were evaluated during patient admission and at 1, 6 and 12 months postoperation or during medical treatment. The surgery group included 37 patients (18 women, 19 men); FEFLDHs were localised at the L3-4 (n=9), L4-5 (n=23) and L5-S1 (n=5) levels. NP was detected in 16 patients before surgery (43%). The medical-treated group included 46 patients (19 women, 27 men); FEFLDHs were localised at the L2-3 (n=7), L3-4 (n=12) and L4-5 (n=27) levels. NP was detected in 20 patients before medical treatment (43%). The most common neuropathic symptom for patients was a burning sensation. NP was found more common in patients who were of at advanced age ( > 65 years) (p=0.019), had a longer clinical duration (p=0.007) or had a foraminal disc herniation (p=0.038). Chronic compression of the dorsal root ganglion by FEFLDH is a significant cause of NP. If surgical treatment is delayed for FEFLDH, the risk of persistent NP may increase.

Dejerine–Roussy syndrome

Pharmaceutical treatment Opiates contain the narcotics morphine, codeine, and papaverine which provide pain relief. Opiates activate μ-opioid receptors in the brain which alter the brain's perception of sensory input, alleviating pain and sometimes inducing pleasure for a short time period. When intravenously administered, opiates can relieve neuropathic pain but only for a time between 4 and 24 hours. After this time window, the pain returns and the patient must be treated again. Although this method of treatment has been proven to reduce pain, the repetitive use of opiates has also been linked to the activation of the brain's reward system and therefore poses a threat of addiction. Heavy doses of opiates can also cause constipation, and respiratory depression. More common side effects include light-headedness, dizziness, sedation, itching, nausea, vomiting, and sweating.

Curative effect research on curing intercostal neuralgia through paravertebral nerve block combined with pregabalin.

This paper aimed to discuss the curative effect and safety of curing intercostal neuralgia through paravertebral nerve block combined with pregabalin. 90 cases of patients diagnosed as intercostal neuralgia were taken as research object. Random number method was used to divide the patients that is conforming to the inclusion criteria and exclusion criteria into 3 groups. 30 cases was in group A (oral lyrica), 30 cases was in group B (paravertebral block only) and 30 cases was in group C (paravertebral block combined with pregabalin). The clinical effect and safety of three groups was compared. The result showed that: visual analogue scale (VAS) and quality of sleep (QS) of three groups of patients after treatment all decreased obviously; group A had slow work, large amount of dosage and many adverse effects; group B had quick work, but the improvement on pain and sleep was not satisfactory; the curative effect of group C was higher than group A and B (p<0.05); 3 groups all had adverse effect, among which group C had the least adverse effect. It can be concluded that paravertebral nerve block combined with pregabalin for curing intercostal neuralgia was superior than single use of pregabalin or paravertebral block and that is worth to promote.

Cancer pain

Analgesics should not be taken "on demand" but "by the clock" (every 3–6 hours), with each dose delivered before the preceding dose has worn off, in doses sufficiently high to ensure continuous pain relief. People taking slow-release morphine should also be provided with immediate-release ("rescue") morphine to use as necessary, for pain spikes (breakthrough pain) that are not suppressed by the regular medication. Oral analgesia is the cheapest and simplest mode of delivery. Other delivery routes such as sublingual, topical, transdermal, parenteral, rectal or spinal should be considered if the need is urgent, or in case of vomiting, impaired swallow, obstruction of the gastrointestinal tract, poor absorption or coma. Current evidence for the effectiveness of fentanyl transdermal patches in controlling chronic cancer pain is weak but they may reduce complaints of constipation compared with oral morphine.

Neuropathic Pain Frequency in Neurology Outpatients: A Multicenter Study.

Neuropathic pain is common, but the frequency of misdiagnosis and irrational treatment is high. The aim of this study is to evaluate the rate of neuropathic pain in neurology outpatient clinics by using valid and reliable scales and review the treatments of patients. The study was conducted for 3 months in eleven tertiary health care facilities. All outpatients were asked about neuropathic pain symptoms. Patients with previous neuropathic pain diagnosis or who have neuropathic pain symptoms were included and asked to fill painDETECT and douleur neuropathic en 4 questions (DN4) questionnaire. Patients whose DN4 score is higher than 3 and/or painDETECT score higher than 13 and/or who are on drugs for neuropathic pain were considered patients with neuropathic pain. The frequency of neuropathic pain was calculated and the treatments of patients with neuropathic pain were recorded. Neuropathic pain frequency was 2.7% (95% CI: 1.5-4.9). The most common cause was diabetic neuropathy. According to painDETECT, the mean overall pain intensity was 5.7±2.4, being lower among patients receiving treatment. Pharmacological neuropathic pain treatment was used by 72.8% of patients and the most common drug was pregabalin. However, 70% of those receiving gabapentinoids were using ineffective doses. Besides, 4.6% of the patients were on medications which are not listed in neuropathic pain treatment guidelines. In our cohort, the neuropathic pain severity was moderate and the frequency was lower than the literature. Although there are many guidelines, high proportion of patients were being treated by ineffective dosages or irrational treatments.

Transdermal buprenorphine controls central neuropathic pain.

A 53-year-old male with peripheral sensorimotor neuropathy suffered an intracerebral hemorrhage resulting in right hemiparesis and hemisensory loss. Three months later, he developed constant and burning pain within the entire right side of his body. He was diagnosed with central pain syndrome and treated with antiepileptics and tricyclic antidepressants. Minimal analgesia was achieved, which was limited by intractable sedation and drowsiness. Patient was then treated with oral opioids (morphine and hydrocodone with acetaminophen) in escalating doses that produced cognitive impairment. After an opioid rotation was attempted, by switching morphine to transdermal fentanyl, there was no pain reduction or improved quality of life. A trial of buprenorphine was initiated, by administering transdermal patches in escalating doses in weekly intervals. Patient's pain was eventually successfully controlled with buprenorphine patch 60 μg/h every 7 days. His self-reported Visual Analogue Scale pain scores decreased from an average of 8/10 to 2/10 or less. Patient's overall function and participation in home activities increased. Buprenorphine is a partial μ-receptor and a κ-δ receptor antagonist known to block NMDA receptors and reduce hyperalgesia secondary to central sensitization.(1) Buprenorphine is also a partial agonist at the opioid receptor-like (ORL-1) receptor, which is found to be analgesic and antinociceptive at the level of the spinal cord.(1,2) The difference in analgesic responses between buprenorphine and other opioids may be due to different receptor G protein interactions and/or selective activation of neuronal K(ATP) channels by buprenorphine.(3) Deficient opening of K(ATP) channels has been shown to mediate neuropathic pain(4); therefore, activation of these channels by buprenorphine may contribute to its analgesic effect in neuropathic pain states wherein other opioids fail. More recently, there have been two case reports in which patients with neuropathic pain of different central etiology were successfully treated with buprenorphine.(5) Despite advances in understanding the pathology related to central pain, effective treatment options are limited. Buprenorphine may be an analgesic option for central pain management when opioids fail to reduce hypersensitivity or when patients exhibit intolerable side effects to other medications.

InternalMed_Harrison

These drugs are useful primarily for patients with neuropathic pain. Phenytoin (Dilantin) and carbamazepine (Tegretol) were first shown to relieve the pain of trigeminal neuralgia. This pain has a characteristic brief, shooting, electric shock–like quality. In fact, anticonvulsants seem to be particularly helpful for pains that have such a lancinating quality. Newer anticonvulsants, gabapentin (Neurontin) and pregabalin (Lyrica), are effective for a broad range of neuropathic pains. Furthermore, because of their favorable side effect profile, these newer anticonvulsants are often used as first-line agents.

Gabapentin enhances the analgesic effect of morphine in healthy volunteers.

The most effective group of drugs for the treatment of severe pain is opioid analgesics. Their use, however, is limited by decreased effects in neuropathic and chronic pain as a result of increased pain and development of tolerance. Gabapentin (GBP) is effective in both experimental models of chronic pain and clinical studies of neuropathic pain. Therefore, we investigated, in a randomized, placebo-controlled, double-blinded study, the pharmacodynamic and pharmacokinetic interaction of GBP and morphine in 12 healthy male volunteers. Morphine (60 mg, controlled release) or placebo was administered at 8:00 AM, and GBP (600 mg) or placebo was administered at 10:00 AM, thus comparing the analgesic effect of placebo + GBP (600 mg) with placebo + placebo and morphine (60 mg) + GBP in comparison to morphine plus placebo by using the cold pressor test. The duration and intensity of the side effects were assessed by using visual analog scales. The analgesic effect was evaluated by the change in the area under the curve (h x %; 0% baseline before Medication 1) of pain tolerance. Placebo + GBP (18.9% x h, 95% confidence interval [CI]: -2.5 to 40.3) did not present any significant analgesic effect compared with placebo + placebo (4.7% x h, 95% CI: -16.7 to 26.1). A significant increase in pain tolerance was observed comparing the combination of morphine and GBP (75.5% x h, 95% CI: 54.0-96.9) with morphine + placebo (40.6% x h, 95% CI: 19. 2-62.0). The observed adverse events after placebo + GBP were not significantly different compared with placebo + placebo. Morphine + placebo led to the expected opioid-mediated side effects. They were significantly more pronounced compared with placebo + placebo but did not differ significantly compared with the combination of morphine + GBP. Concerning the pharmacokinetic variables of morphine and its glucuronides, no significant difference between morphine + placebo and morphine + GBP was observed, whereas the area under the curve of GBP (43.9 +/- 5.3 vs 63.4 +/- 16.2 microg. h(-1). mL(-1), P < 0.05) significantly increased, and apparent oral clearance (230.8 +/- 29.4 mL/min vs 178 +/- 97.9 mL/min, P = 0.06) and apparent renal clearance (86.9 +/- 20.6 vs 73.0 +/- 24.2 mL/min, P = 0.067) of GBP decreased when morphine was administered concomitantly. These results suggest two different sites for the pharmacokinetic interaction-one at the level of absorption and the other at the level of elimination. Our study reveals both a pharmacodynamic and pharmacokinetic interaction between morphine and GBP, leading to an increased analgesic effect of morphine + GBP. These results and the good tolerability of GBP should favor clinical trials investigating the clinical relevance of the combination of morphine and GBP for treating severe pain. In a randomized, placebo-controlled, double-blinded trial with 12 healthy volunteers, we studied the interaction of morphine and gabapentin using the cold pressor test. The anticonvulsant gabapentin enhanced the acute analgesic effect of morphine. Furthermore, the plasma concentration of gabapentin was increased when morphine was administered concomitantly. Therefore, the well tolerated combination of gabapentin and morphine may improve pain therapy, especially in pain states, like chronic and neuropathic pain, which respond poorly to opioids.


The question would be more of neurology. It is a claude bernard horner syndrome and probably the correct one is 1. But for safety's sake it is better to have it checked by a neurologist.

The question would be more of neurology. It is a claude bernard horner syndrome and probably [HIDDEN]. But for safety's sake it is better to have it checked by a neurologist.

Juan is 60 years old, has been smoking 2 packs/day for years and has reported a persistent cough for the last 6 months. He notes that his left eyelid is more droopy and that the pupil of this eye is smaller. John reports that the medial side of his left hand is numb and with less strength. His physician checks for palpebral ptosis and left miosis; he checks that he can close both eyelids symmetrically and that both pupils respond correctly to light. In addition, he checks that there is no sweating from the left hemiface, that he feels less prickling on the inner surface of the left hand and that he has less strength in the grip of the left hand. Regarding the ocular symptomatology, where is the lesion located?

Sympathetic fibers, at some level that would span from the hypothalamus to the interinedio-lateral Clark's column of the dorsal medulla.

Left common ocular motor nerve in the midbrain.

Edinger-Westphal nucleus above the left common ocular motor nerve nucleus.

Parasympathetic fibers, at some level ranging from the Edinger-Westphal nucleus to the constrictor muscle of the left pupil.

Oculomotor nerve

All these branches enter the muscles on their ocular surfaces, with the exception of the nerve to the inferior oblique, which enters the muscle at its posterior border. Nuclei The oculomotor nerve (CN III) arises from the anterior aspect of mesencephalon (midbrain). There are two nuclei for the oculomotor nerve: The oculomotor nucleus originates at the level of the superior colliculus. The muscles it controls are the striated muscle in levator palpebrae superioris and other extraocular muscles except for the superior oblique muscle and the lateral rectus muscle. The Edinger-Westphal nucleus supplies parasympathetic fibers to the eye via the ciliary ganglion, and thus controls the sphincter pupillae muscle (affecting pupil constriction) and the ciliary muscle (affecting accommodation).

Pupillary light reflex

Schematic Referring to the neural pathway schematic diagram, the entire pupillary light reflex system can be visualized as having eight neural segments, numbered 1 through 8. Odd-numbered segments 1, 3, 5, and 7 are on the left. Even-numbered segments 2, 4, 6, and 8 are on the right. Segments 1 and 2 each includes both the retina and the optic nerve (cranial Nerve #2). Segments 3 and 4 are nerve fibers that cross from the pretectal nucleus on one side to the Edinger-Westphal nucleus on the contralateral side. Segments 5 and 6 are fibers that connect the pretectal nucleus on one side to the Edinger-Westphal nucleus on the same side. Segments 3, 4, 5, and 6 are all located within a compact region within the midbrain. Segments 7 and 8 each contains parasympathetic fibers that courses from the Edinger-Westphal nucleus, through the ciliary ganglion, along the oculomotor nerve (cranial nerve #3), to the ciliary sphincter, the muscular structure within the iris.

Parasympathetic nervous system

The oculomotor nerve is responsible for a number of parasympathetic functions related to the eye. The oculomotor PNS fibers originate in the Edinger-Westphal nucleus in the central nervous system and travel through the superior orbital fissure to synapse in the ciliary ganglion located just behind the orbit (eye). From the ciliary ganglion the postganglionic parasympathetic fibers leave via short ciliary nerve fibers, a continuation of the nasociliary nerve (a branch of ophthalmic division of the trigeminal nerve (CN V1)). The short ciliary nerves innervate the orbit to control the ciliary muscle (responsible for accommodation) and the iris sphincter muscle, which is responsible for miosis or constriction of the pupil (in response to light or accommodation). There are two motors that are part of the oculomotor nerve known as the somatic motor and visceral motor. The somatic motor is responsible for moving the eye in precise motions and for keeping the eye fixated on an object. The

Neuroanatomy, Brainstem -- Nerves -- Midbrain

The Oculomotor nerve (cranial nerve III) – Arises from the oculomotor sulcus on the medial portion of the crus cerebri. It is a motor nerve that receives inputs from two nuclei. The first nucleus is the oculomotor nucleus; it serves as its main motor nucleus and is in the anterior midline of the periaqueductal grey at the level of the superior colliculus. The second nucleus is the Edinger-Westphal nucleus, which provides parasympathetic motor inputs. The somatic motor fibers from the oculomotor nucleus provide innervation to all the extraocular muscles, with the exceptions of the superior oblique and lateral rectus muscles. The parasympathetic motor fibers of the Edinger-Westphal nucleus provide innervation to the ciliary muscles and constrictor pupillae after passing through the ciliary ganglion.

Neuroanatomy, Vestibular Pathways -- Nerves -- Vestibulocochlear Nerve

CN III, IV, and VI nerves innervate the six extraocular muscles that control eye movements in response to head movements. When the head turns to the left, vestibular information initiates its journey from the left semicircular canal via vestibular nerve fibers and proceeds to the ipsilateral medial and superior vestibular nuclei. Then, excited neurons in the left superior and medial vestibular nuclei send signals to the right CN VI nucleus. The right CN VI innervates the right lateral rectus muscle to contract and direct the gaze to the right. Another nerve fiber projects from the CN VI nucleus and ascends via the MLF toward the left CN III nucleus. When stimulated, the oculomotor nerve results in the medial rectus muscle contraction and allows the left eye to gaze to the right. Inhibitory nerve fibers also proceed from the medial vestibular nucleus to the left CN VI nucleus, rendering the left lateral rectus and right medial rectus muscles to relax. The result of these combined counteracting effects is a smooth, coordinated eye movement toward the opposite direction, and thus a steady visual field with head-turning. The trochlear nerves innervate the contralateral superior oblique muscle and stimulate the muscle to contract and make eye movements via lateral rotation, intorsion, and depression. [8] [24]

Anatomy, Head and Neck: Eye Nerves -- Structure and Function -- Parasympathetic nervous system

The parasympathetic nervous system causes pupillary constriction through a process called miosis. The parasympathetic nerve fibers start at the first neuron called the Edinger-Westphal nucleus. This neuron's nerve fibers span to the ciliary ganglion by traveling on the oculomotor nerve. After the ciliary ganglion, the second neuron is from the short ciliary nerves to the sphincter pupillae muscles. When the sphincter pupillae muscle contract, it will cause the constriction of the pupils. [7]

Ciliary body

Nerve supply The parasympathetic innervation of the ciliary body is the most clearly understood. Presynaptic parasympathetic signals that originate in the Edinger-Westphal nucleus are carried by cranial nerve III (the oculomotor nerve) and travel through the ciliary ganglion. Postsynaptic fibers from the ciliary ganglion form the short ciliary nerves. Parasympathetic activation of the M3 muscarinic receptors causes ciliary muscle contraction, the effect of contraction is to decrease the diameter of the ring of ciliary muscle. The parasympathetic tone is dominant when a higher degree of accommodation of the lens is required, such as reading a book. The ciliary body is also known to receive sympathetic innervation via long ciliary nerves. When test subjects are startled, their eyes automatically adjust for distance vision.

Roots of the ciliary ganglion

Presynaptic parasympathetic fibers originate in the Edinger-Westphal nucleus, the parasympathetic motor nucleus associated with the oculomotor nucleus in the brainstem. Axons from the Edinger-Westphal nucleus and the oculomotor nucleus run together in the brainstem and exit together as the oculomotor nerve. The oculomotor nerve passes through the lateral wall of the cavernous sinus and enters the orbit through the superior orbital fissure. It divides into branches that innervate the levator palpebrae superioris and four of the six extraocular muscles. Parasympathetic fibers initially run in the inferior division of the oculomotor nerve. They exit as one or two short “motor roots” that synapse in the ciliary ganglion.

Pupillary Light Reflex -- Anatomy and Physiology

Light travels through the cornea, anterior chamber, pupil, lens, and the posterior chamber, eventually reaching the retina. Photoreceptor cells in the outer layers of the retina, which are called rods and cones, convert light stimuli into neuronal impulses. These signals are then relayed to the bipolar cells, which interact with ganglion cells, which in turn coalesce to form the optic disc and optic nerve (CN II). The optic nerve sends impulses to the brain for further processing and image recognition. [1] These are the first steps of the pupillary light reflex afferent pathway. The optic nerve then forms the optic chiasm, which diverges into a left and right optic tract. At the optic chiasm, nasal retinal fibers will cross to the contralateral side of the optic tract, and the temporal retinal fibers continue on the ipsilateral side. Thus, the right optic tract will contain temporal retinal fibers from the right eye, as well as nasal retinal fibers from the left eye. The optic tracts join the brachium of the superior colliculus, and then signals travel to the pretectal area of the midbrain. Each pretectal area sends bilateral signals to the preganglionic parasympathetic nuclei in the midbrain called Edinger-Westphal nuclei. [2] [3] There are a minority of axons that go to the hypothalamus and the olivary pretectal nucleus (OPN). [4] Efferent parasympathetic preganglionic fibers travel on the oculomotor nerve and synapse with the ciliary ganglion, which sends postganglionic axons to directly innervate the iris sphincter muscles. The contraction of the iris sphincter muscles leads to pupillary constriction (miosis). [3] This extensive pathway is being tested when a light is shined in the eyes. And, because of the crossing fibers, there is not only a direct pupillary reflex but also a consensual pupillary light reflex. Of note, the pupillary dark reflex involves a separate pathway, which ends with sympathetic fibers from long ciliary nerves innervating the dilator pupillae muscle.

Isolated Horner syndrome as a rare initial presentation of nasopharyngeal carcinoma: a case report.

Horner syndrome refers to a set of clinical presentations resulting from disruption of sympathetic innervation to the eye and adnexa. Classically, the clinical triad consists of ipsilateral blepharoptosis, pupillary miosis, and facial anhidrosis. Ocular sympathetic denervation may signify life-threatening causes. Timely investigation and accurate diagnosis are essential in patients with oculosympathetic denervation. A 33-year-old Asian man with a heavy smoking habit presented with a 3-week history of left ptosis and no other complaints. His visual acuity was 20/20 bilaterally. An ophthalmic examination was significant for mild ptosis of his left eyelid and anisocoria (smaller left pupil), which was greater in the dark. Both pupils reacted to light briskly without an afferent pupillary defect. Anhidrosis was found on the medial side of the left forehead. A 10% cocaine test was positive. At his first visit, neurologic examination was unremarkable. Comprehensive radiological investigations were scheduled for a left-sided isolated Horner syndrome. Two weeks after his first visit, he experienced a left-sided headache along with ipsilateral Horner syndrome. Neurologic examination revealed hypoesthesia in the left cranial nerve V<sub1-3</sub territories. Emergent computed tomography angiography was suspected for petrous part of the left internal carotid artery (ICA) dissection. Magnetic resonance imaging demonstrated an enhancing infiltrative lesion with its epicenter at the left sphenoid bone. The lesion encased the left ICA and invaded the left Meckel cave. Rhinoscopy with incisional biopsy revealed squamous cell nasopharyngeal carcinoma. This case involved an unusual initial presentation of nasopharyngeal carcinoma: isolated Horner syndrome with clinical progression to adjacent structures. Infiltration involving the Meckel cave and ICA at the foramen lacerum can present as postganglionic Horner syndrome associated with trigeminal pain and hypoesthesia. These clinical findings may mimic carotid artery dissection on computed tomography angiography. Detailed magnetic resonance imaging with careful attention to the skull base should be performed.

Cranial Nerve III Palsy -- Introduction

The third cranial nerve is also known as oculomotor nerve and has 2 major components: Outer parasympathetic fibers that supply the ciliary muscles and the sphincter pupillae Inner somatic fibers that supply the levator palpebrae superioris in the eyelid (which retracts the upper eyelid) and the 4 extraocular muscles (superior, middle, inferior recti, and inferior oblique). LR6(SO4)3 is a simple mnemonic representing the innervation of the extraocular muscles. It stands for: LR6: Lateral rectus muscle which is supplied by the sixth cranial nerve SO4: Superior oblique muscle which is supplied by the fourth cranial nerve 3: The third cranial nerve supplies other extraocular muscles

[A 55-year-old man with prostate cancer, papilledema, and multiple cranial nerve palsies].

We report a 55-year-old man with papilledema and multiple cranial nerve palsies. He was well until 52 years of age when there was an onset of progressive difficulty in initiating urination; he visited the urology service of our hospital where a diagnosis of prostate cancer was made; the cancer was invading the bladder and was metastasizing to lymph nodes and bones. He was treated with oochiectomy and estrogen preparations with some improvement in his symptoms. Two years later, he developed difficulty in urination again, and transurethral resection of the tumor was performed in 1991. In December 1991, he noted tingling and numb sensation in his left face, which had become progressive worse within the next one month, and he developed blepharoptosis and deafness all on the left side. He was admitted to the urology service on February 4, 1992, and a neurological consultation was asked. On physical examination, general findings were unremarkable, except for lymph node enlargements of about 0.5 to 1.0 mm in size in cervical and inguinal regions. On neurologic examination, he was alert with normal mental activities; higher cerebral functions were intact. He had normal vision and visual fields, however, papilledema was present bilaterally; pupils and light reactions were normal. Extraocular muscles were intact on the right side, however, moderate restriction was noted in the left eye in that all the extraocular muscles except for the medial rectus were weak; blepharoptosis was noted on the left; no nystagmus was present. The sensation was diminished in the left face, and left facial paresis of the peripheral type was also noted; the taste sensation was also diminished in the left anterior two thirds of the tongue. He had sensorineural deafness on the left side. The other cranial nerves appeared intact. He walked normally; no weakness or muscle atrophy was noted; muscle tone was normal and no ataxia was observed. Deep reflexes were normally elicited and symmetric; the plantar response was flexor. No meningeal signs were present. Laboratory examination revealed following abnormalities: Hb 7.1 g/dl, platelet 47,000/cmm, WBC3,800/cmm, LDH 950IU/l, PAP232ng/ml (normal less than 1.6), PA2.631ng/ml (normal less than 7.4); a small amount of effusion was noted in the left pleural cavity; cytological examination of the fluid was class V. A cranial CT scan as well as MRI were entirely normal, as was the spinal tap. He was treated with glycerol, however, there was progressive increase in the pleural effusion, and he developed dyspnea; moist rale had become audible in the end of February.(ABSTRACT TRUNCATED AT 400 WORDS)

Anatomy, Head and Neck: Eye Nerves -- Nerves

There are six cranial nerves and nerve fibers from the autonomic nervous system. Optic nerve Oculomotor nerve Short ciliary nerve (parasympathetic nervous system) Trochlear nerve Trigeminal nerve (ophthalmic branch) Abducens nerve Facial nerve Long ciliary nerve (sympathetic nervous system)

Physiology_Levy

Fig. 11.1 ). Hence, this part of the autonomic nervous system is sometimes called the craniosacral division. The cranial nerve nuclei that contain parasympathetic preganglionic neurons are the Edinger-Westphal nucleus (cranial nerve III), the superior (cranial nerve VII) and inferior (cranial nerve IX) salivatory nuclei, and the dorsal motor nucleus of the vagus and nucleus ambiguus (cranial nerve X). Postganglionic parasympathetic cells are located in cranial ganglia, including the ciliary ganglion (preganglionic input is from the Edinger-Westphal nucleus), the pterygopalatine and submandibular ganglia (input is from the superior salivatory nucleus), and the otic ganglion (input is from the inferior salivatory nucleus). The ciliary ganglion innervates the pupillary sphincter and ciliary muscles in the eye. The pterygopalatine ganglion supplies the lacrimal gland, as well as glands in the nasal and oral pharynx. The submandibular ganglion projects to the submandibular and sublingual

Pupillary light reflex

The pupillary light reflex neural pathway on each side has an afferent limb and two efferent limbs. The afferent limb has nerve fibers running within the optic nerve (CN II). Each efferent limb has nerve fibers running along the oculomotor nerve (CN III). The afferent limb carries sensory input. Anatomically, the afferent limb consists of the retina, the optic nerve, and the pretectal nucleus in the midbrain, at level of superior colliculus. Ganglion cells of the retina project fibers through the optic nerve to the ipsilateral pretectal nucleus. The efferent limb is the pupillary motor output from the pretectal nucleus to the ciliary sphincter muscle of the iris. The pretectal nucleus projects crossed and uncrossed fibers to the ipsilateral and contralateral Edinger-Westphal nuclei, which are also located in the midbrain. Each Edinger-Westphal nucleus gives rise to preganglionic parasympathetic fibers which exit with CN III and synapse with postganglionic parasympathetic neurons in

Permanent paralysis at sites of dermal exposure to chlorpyrifos.

Poisoning with organophosphate pesticides can cause sensory and motor neuropathy with permanent paralysis. Paralysis at the site of dermal exposure has not been reported. A 61-year-old carpenter sprayed a nest of termites with an insecticide containing chlorpyrifos without protective equipment and with direct contact of pesticide solution to hands, lower arms, feet, and lower legs, as well as inhalation of vapors from spraying. After 30 min he became ill with nausea, abdominal cramping, arm and leg weakness, bilateral shoulder pain, chest pain, and numbness in the left hand and arm. At a hospital, he was treated with atropine 1 mg IV and pralidoxime Cl 2 g IV There was 0/5 strength in the hands and wrists and 3/5 elsewhere, a left peritoneal palsy, and urinary retention. He was transferred to a tertiary care hospital where paralysis persisted. Electromyogram studies documented widespread peripheral neuropathy. With continued progression of neuropathy, pralidoxime was repeated on the third day. By day 12, motor strength improved except for the hands and left lower leg. Right interosseous muscle strength was 1/5 and left was 0/5. Right-hand grip was 2/5, and left-hand grip was 0/5. He was transferred to a rehabilitation center. He never regained use of his hands and was disabled from employment as a carpenter. There was a disturbed gait, with inability to clear his left foot with walking. Urinary retention persisted and required self-catherization. Dermal exposure of the hands and feet to chlorpyrifos was associated with atrophy and permanent paralysis of exposed areas. The importance of protective equipment is emphasized.

Anatomy, Head and Neck: Eye Nerves -- Structure and Function -- Abducens Nerve (CN VI)

The abducens nerve innerves only one muscle in the eye. This muscle is the lateral rectus muscle. When this muscle contracts, it causes the eye to abduct. [5]

[A 56-year-old man with fever, backache and tetraparesis].

We report a 56-year-old man who developed progressive paraparesis. He was apparently well, except for left Bell's palsy which developed on May 9 of 1994, for which he received stellate ganglion block on the left side more than ten times until July 2nd of 1994, when he noted pain in his left shoulder and in his lumbar region. On July 5th, he noted some difficulty in urination. On July 6th, he noted tingling sensation in his four extremities and difficulty in gait. He was admitted to another hospital where he was treated with intravenous infusion of glycerol. After this treatment, his gait and sensory disturbance showed some improvement, however, on July 7th, his shoulder and lumbar pain worsened, and he became unable to stand. His temperature went up to 39 degrees C on the next day. Lumbar CSF on that day contained 119 cells/microliters, 112 mg/dl of protein, and 53 mg/dl of sugar. He was transferred to our hospital on July 14th. His past medical history revealed that he had suffered from frequent bouts of osteomyelitis since the age of 13 years. He was operated on several times on osteomyelitis. He had been treated on his tooth ache until shortly before the onset of the present illness. He also received steroid hormone for his Bell's palsy. On admission, his consciousness varied from alert to stupor. His BP was 150/100 mmHg, HR 98/min and regular, BT 39.4 degrees C. The bulbar conjunctiva appeared somewhat icteric. Otherwise, general physical examination was unremarkable. On neurologic examination, there was no apparent dementia. Higher cerebral functions appeared intact. The optic discs were flat. Pupils were round and isocoric reacting to light and accommodation promptly. Ocular movements were full without nystagmus. Some exophthalmos was noted bilaterally. The sensation of the face and facial muscles were intact. The remaining cranial nerves also appeared intact. Nuchal rigidity was present. He was unable to stand or walk. Muscle strength was markedly diminished in all four limbs; manual muscle testing revealed 1 to 2/5 weakness in both upper and lower extremities bilaterally. Muscle stretch reflexes were decreased or lost in both upper and lower limbs, but the plantar response was extensor on the right. Sensation appeared to be diminished in legs, but detail was not clear because of disturbance of consciousness. Pertinent laboratory findings were as follows: WBC 12,800/microliter, GPT 58 IU/l, total bilirubin 2.65 mg/dl, and CRP 16.8 mg/dl. Cerebrospinal fluid contained 34 cells/microliter (approximately two thirds were neutrophils), RBC 1,110/microliter, 2,949 mg/dl of protein, and 119 mg/dl of glucose; stapylococcus aureus was cultured from the CSF. Myelogram showed a filling defect in the anterior epidural space between the low thoracic and the upper lumbar region. The patient was treated with cephotaxim, aminobenzyl penicillin, and chloramphenicol. On the second hospital day, his BT was still 39 degrees C and he was agitated His weakness was worse than the previous day. Spinal MRI was attempted; as he was agitated 5 mg of diazepam was given intravenously at 4 PM. His respiration was rapid and somewhat shallow. At 6 PM, gadolinium DTPA was injected intravenously; at that time, he was breathing and pupils were 3 mm on both sides. At 6:35 PM, an examiner noted that he stopped breathing; the left pupil was dilated to 5 mm. Cardiopulmonary resuscitation was initiated immediately, and intubation was performed. He was placed on a respirator. His blood pressure did not reach 100 mmHg; he was in deep coma. Cardiac arrest occurred at 8:53 AM on the next morning. The patient was discussed in a neurological CPC. Most of the participants thought that the patient had either spinal epidural empyema or spinal subdural abscess. The question was what might be the original focus of infection. Three possibilities were considered, i.e., stellate ganglion block, teeth infection, and osteomyelitis...

Anatomy, Head and Neck, Eye -- Muscles

Six extrinsic eye muscles that move each eye: (1) superior rectus, (2) inferior rectus, (3) lateral rectus, (4) medial rectus, (5) superior oblique, and (6) inferior oblique. Lateral rectus is innervated by trochlear and superior oblique is innervated by abducens nerve; The oculomotor nerve innervates the remaining four muscles. The motor units in these muscles tend to be small with neurons serving only two or three muscle fibers at times. Such small motor units allow precise and rapid eye movement. Portions of the brainstem and cerebellum coordinate eye movements.

A Case Report of Herpes Zoster-Associated Bickerstaff Brainstem Encephalitis.

Bickerstaff brainstem encephalitis (BBE) is a rare demyelinating disease of the central nervous system (CNS) that is caused by a direct viral infection or secondary autoimmune responses. BBE secondary to Herpes zoster has rarely been reported. A 68-year-old man developed a painful vesicular rash and drooping eyelid on the left side of his face for 20 days. Physical examination revealed left-sided blepharoptosis and crusted erythema on the left front side of his face, left upper eyelid, and left nasal tip. Neurological examination showed impaired sensation over the left side of his face and cheek. His left pupil was dilated (4mm compared to 2mm on the right side), and the Pupillary light reflection (PLR) was absent, with an ocular movement disorder (limited adduction) and diplopia. Brain imaging did not reveal abnormalities. Cerebrospinal fluid (CSF) examination showed leukocytosis and increased protein levels. He was treated with intravenous acyclovir for 7 days, but developed disturbance of consciousness and right limb weakness. Neurological examination revealed right lower limb hypoesthesia. The Heel-Knee-Shin test was positive on the left side, and Babinski's sign was present on the right side. He was diagnosed with Bickerstaff brainstem encephalitis caused by herpes zoster. After 2 days of intravenous acyclovir combined with intravenous immune globulin (IVIG), the patient developed acute kidney injury (AKI). Then, his treatment was changed to systemic steroids. At the 3-month follow-up, his pupils were bilaterally equal and reactive to light, and there was a significant improvement in ocular motility and ptosis. At the 6-month follow-up, his diplopia had completely resolved. BBE associated with herpes zoster is very rare and can be overlooked. Dermatologists should be aware of the expanding spectrum of neurological complications caused by varicella zoster virus (VZV) infections to aid early diagnosis and treatment.

Anatomy, Head and Neck: Eye Inferior Oblique Muscles -- Nerves

The inferior division of cranial nerve III, also known as the oculomotor nerve, runs inferolaterally along the inferior rectus to innervate the inferior oblique muscle. The nerve is approximately 27 mm long, running from orbital apex to the inferior oblique muscle. [6] The nerve to the inferior oblique is the longest branch of the inferior division of the oculomotor nerve. It enters the muscle through its orbital surface. [2] The nerve has been measured to be approximately 1.04mm on the right and 1.07 mm on the left. [2]

Ptosis (eyelid)

Ptosis caused by oculomotor palsy can be unilateral or bilateral, as the subnucleus to the levator muscle is a shared, midline structure in the brainstem. In cases in which the palsy is caused by the compression of the nerve by a tumor or aneurysm, it is highly likely to result in an abnormal ipsilateral papillary response and a larger pupil. Surgical third nerve palsy is characterized by a sudden onset of unilateral ptosis and an enlarged or sluggish pupil to the light. In this case, imaging tests such as CTs or MRIs should be considered. Medical third nerve palsy, contrary to surgical third nerve palsy, usually does not affect the pupil and it tends to slowly improve in several weeks. Surgery to correct ptosis due to medical third nerve palsy is normally considered only if the improvement of ptosis and ocular motility are unsatisfactory after half a year. Patients with third nerve palsy tend to have diminished or absent function of the levator.

[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age].

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.

Anatomy, Head and Neck: Eye Nerves -- Clinical Significance -- Oculomotor Nerve

Motor : Compromised of the motor function of the oculomotor nerve will manifest as a down and out gaze with ptosis. The reason behind this eye position is the unopposed action of the trochlear and abducens nerve pulling the eye inferiorly and laterally, respectively. Causes of compromise to the motor function of the oculomotor nerve can be from ischemia from vascular disease or due to the build-up of sorbitol from diabetes. This ischemia is due to poor perfusion. The motor nerve fibers of the oculomotor nerve can be affected along with the parasympathetic nerve fibers with severe compression. The compression of the oculomotor nerve first affects the parasympathetic nerve fibers; then, it can progress to compression of the arterial blood supply.

Physiology_Levy

Fig. 8.27 ). The depolarized hair cells cause increased activity in the left vestibular afferent fibers and thereby excite neurons of the left medial vestibular nucleus. These include excitatory neurons that project to the contralateral abducens nucleus and synapse with both motor neurons and internuclear neurons. Excitation of the motor neurons leads to contraction of the right lateral rectus muscle and rotation of the right eye to the right, whereas excitation of the internuclear neurons of the right abducens nucleus leads to excitation of the medial rectus motor neurons in the left oculomotor nucleus, thus causing the left eye to rotate to the right as well.

A rare presentation of myxofibrosarcoma as a Pancoast tumor: a case report.

Myxofibrosarcoma is an aggressive soft tissue neoplasm, classified as a variant of malignant fibrous histiocytoma. Most often, it occurs in middle to late adult life peaking in the seventh decade and involving the lower extremities (77%), trunk (12%), and retroperitoneum or mediastinum (8%). We report the first case of thoracic myxofibrosarcoma presenting as a Pancoast tumor. A 48-year-old non-tobacco smoking African-American man presented with a slow-growing mass in his neck along with 11 kg weight loss over 9 months. A review of his systems was positive for hoarseness and lowgrade intermittent fever without any shortness of breath or cough. A physical examination revealed a mass on the left side of his neck superior to his sternoclavicular joint measuring 3 × 3 × 1 cm. He had ptosis and miosis of his left eye. His breath sounds were decreased and coarse at the left apex. A neurological examination revealed 3/5 strength in his left upper arm. The remainder of the physical examination was unremarkable. Ultrasound of his neck showed an ill-defined heterogeneous mass lateral to his left thyroid lobe. A computed tomography scan of his chest showed a large multiloculated pleural-based mass in his left lung surrounding the adjacent neurovascular structures. A percutaneous biopsy was non-diagnostic. Subsequently, he underwent a left thoracotomy with biopsy. The mass extended from his anterior mediastinum medially at the level of the pulmonary trunk, superiorly into the superior sulcus and posteriorly into his chest wall. Surgical pathology confirmed the diagnosis of myxofibrosarcoma. Here we present a case of Pancoast tumor with myxofibrosarcoma as the underlying etiology. Pancoast syndrome generally entails an infiltrating lesion in the superior sulcus presenting with upper extremity pain, atrophy of the hand muscles, and Horner's syndrome. The differential diagnosis of Pancoast syndrome includes inflammatory and infectious etiologies, as well as neoplasms of benign and malignant nature. Of the neoplasms implicated, the most common are non-small cell lung carcinomas; myxofibrosarcoma presenting as a Pancoast tumor has not been reported in the literature.

Anatomy, Head and Neck: Eye Inferior Rectus Muscle -- Nerves

Additionally, the parasympathetic innervation of the sphincter pupillae and ciliary muscle travels with the branch of the lower division of cranial nerve III that supplies the inferior oblique muscle, and this bundle passes near the inferior rectus muscle. This anatomy has important surgical considerations that will be explained further. [2]

[A 37-year-old man with memory loss, homonymous hemianopsia, and elevation of anti-herpes simplex virus antibody titer].

We report a 37-year-old man who presented memory loss, homonymous right hemianopsia, and elevation of anti-herpes simplex antibody titer. He had an auto accident in January 1992 in that the car he was driving slipped down a 3 m slope; his car was severely damaged, however, he himself was not injured. Shortly after this accident, he went out of his house less often than before, and he noted some difficulty in his vision. He changed his glasses twice, but his vision was unchanged. In July of 1992, he had an onset of difficulty in recent memory and disorientation to time. He also noted diplopia, and difficulty in seeing objects in his right visual field. He was admitted to our hospital on August 26 of the same year. General physical examination was unremarkable. On neurologic examination, he was alert but disoriented to time and place; calculation was also impaired. Mini-mental state examination was 18/30. He had no aphasia, apraxia, or agnosia. He showed a tendency to neglect his left side. Optic fundi and visual acuity were normal; right homonymous hemianopsia was present. Ocular movement was moderately restricted to most of the directions; pupils were isocoric and reacted to light promptly. He complained of diplopia in right gaze, and monocular nystagmus was induced in his right eye upon right lateral gaze. Trigeminal nerves appeared intact. Minimum left facial weakness was present. The remaining of the cranial nerves appeared intact. His gait was wide-based and tandem gait was impossible. Muscle strength was normal as was the muscle tone. Finger to nose and heel to knee tests were done normally.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic connections to the fifth and sixth cranial nerves.

Thirty additional parasellar gross dissections and light microscopic examinations have been carried out, confirming a previous observation that the sympathetic nerve or nerves running with the carotid artery gives off a multitude of fine branches at irregular intervals on the way up, but the largest residual component joins the sixth cranial nerve and leaves to join the first division of the fifth cranial nerve. No similar fibers can be found by us to the sympathetic in the neck results in a Horner's syndrome and that section of the ophthalmic artery at its point of departure from the carotid does not result in any part of Horner's syndrome nor does secretion of the external, internal or common corotid in the neck, it is assumed that these fibers process the functions the absence of which result in Horner's syndrome.

Pupillary light reflex

are also located in the midbrain. Each Edinger-Westphal nucleus gives rise to preganglionic parasympathetic fibers which exit with CN III and synapse with postganglionic parasympathetic neurons in the ciliary ganglion. Postganglionic nerve fibers leave the ciliary ganglion to innervate the ciliary sphincter. Each afferent limb has two efferent limbs, one ipsilateral and one contralateral. The ipsilateral efferent limb transmits nerve signals for direct light reflex of the ipsilateral pupil. The contralateral efferent limb causes consensual light reflex of the contralateral pupil.

The inferior division of the oculomotor nerve also carries parasympathetic fibers along the optic nerve to the ciliary ganglion. These fibers innervate the sphincter pupillae and ciliary muscles. [2] [7]

[A case of hemi-hyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction].

A case of hemihyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction is reported. A 55-year-old hypertensive man developed right hemiparesis with slight dysarthria and nausea upon awaking. The right side of his face and right upper limb and trunk to the level of the Th8-9 territory showed hyperhidrosis, which disappeared in a week. Ocular motor examination revealed that during forward gaze with the left eye fixing, the right eye deviated outward. The patient was able to adduct the right eye to midposition with the right eye fixing. Rightward gaze elicited full abduction and right-beating nystagmus of the right eye, but the left eye did not adduct. When he attempted to gaze leftward, both eyes made the full excursion, but saccades were slow in that direction. Convergence was intact. Vertical gaze was full, and he did not show Horner's sign. This ocular sign, non-paralytic pontine exotropia, disappeared three days later. T2-weighted spin echo magnetic resonance imaging disclosed a small lesion with high intensity in the inner side of the left middle pons. This hyperhidrosis was thought to be caused by destruction of inhibitory fibers thermoregulating sweating. These findings suggest that at the level of the middle pons inhibitory fibers descend along the inner side of facilitatory fibers thermoregulating sweating, which are speculated to descend the dorso-lateral part of the pontine tegmentum. These findings also suggest that lesions of non-paralytic pontine exotropia may be located in the paramedian pontine reticular formation rostral to the abducens nucleus with ipsilateral medial longitudinal fasciculus lesion, but further investigation is necessary.