The virus is thought to be latent in the trigeminal ganglia and symptoms hyperthyroidism discount 16 mg betahistine, with reactivation symptoms pulmonary embolism generic betahistine 16mg fast delivery, to infect the nose and then the olfactory tract symptoms xanax withdrawal cheap betahistine 16mg amex. Alternatively medicine jewelry discount betahistine 16 mg, with reactivation in the trigeminal ganglia medications medicaid covers discount betahistine 16 mg without a prescription, the infection may spread along nerve fibers that innervate the leptomeninges of the anterior and middle fossae medicine research buy generic betahistine 16mg on-line. The lack of lesions in the olfactory bulbs in as many as 40 percent of fatal cases (Esiri) is a point in favor of the second pathway symptoms 4-5 weeks pregnant buy 16mg betahistine visa. Diagnosis Acute herpes simplex encephalitis must be distinguished from other types of viral encephalitis symptoms 4dp5dt betahistine 16mg generic, from acute hemorrhagic leukoencephalitis of Weston Hurst (page 792), and from subdural empyema, cerebral abscess, cerebral venous thrombosis, and septic embolism (Chap. When aphasia is the initial man- Herpes Simplex Encephalitis this is the commonest and gravest form of acute encephalitis. About 2000 cases occur yearly in the United States, accounting for about 10 percent of all cases of encephalitis in this country. Between 30 and 70 percent are fatal, and the majority of patients who survive are left with serious neurologic abnormalities. The type 2 virus may also cause acute generalized encephalitis, usually in the neonate and in relation to genital herpetic infection in the mother. Type 2 infection in the adult may cause an aseptic meningitis and sometimes a polyradiculitis or myelitis, again in association with a recent genital herpes infection. Exceptionally, the localized adult type of encephalitis is caused by the type 2 virus and the diffuse neonatal encephalitis by type 1. Spinal fluid that contains a large number of red cells may be attributed to a ruptured saccular aneurysm. T1-weighted images demonstrate areas of low signal intensity with surrounding edema and sometimes with scattered areas of hemorrhage occupying the inferior parts of the frontal and temporal lobes. Almost always the lesions enhance with contrast infusion or with gadolinium, indicating cortical and pial abnormalities of the blood-brain barrier. It should be noted that these destructive lesions are almost unique among the viral encephalitides, being seen only occasionally in other viral infections of the brain, among them La Crosse encephalitis in children (McJunkin et al). A rising titer of neutralizing antibodies can be demonstrated from the acute to the convalescent stage, but this is not of diagnostic help in the acutely ill patient and may not be significant in patients with recurrent herpes infections of the oral mucosa. In the experience of Lakeman and colleagues, the test was 98 percent positive in cases proven by cultures of brain biopsy material and gave 6 percent false-positives. False-negative tests are most likely to occur in the first 48 h of febrile infection. A collaborative study sponsored by the National Institutes of Health and also a Swedish study indicated that the antiviral agent acyclovir significantly reduces both mortality and morbidity from the disease (Whitley et al; Skoldenberg et al). Ё For this reason, it is our practice to initiate treatment while confirmatory testing is being carried out. Acyclovir is given intravenously in a dosage of 30 mg/kg per day and continued for 10 to 14 days in order to prevent relapse. Acyclovir carries little risk and can be discontinued if further clinical or laboratory features point to another diagnosis. The main problems that arise from the drug are local irritation of the veins used for infusion, mild elevation of hepatic enzymes, or transient impairment of renal function. Nausea, vomiting, tremor, or an encephalopathy that is difficult to distinguish from the encephalitis itself occur in a very few patients. The matter of relapse after treatment with acyclovir has been recognized increasingly, particularly in children. Several potential mechanisms have been suggested by Tiege and colleagues, includ` ing an immune-mediated inflammatory response, but treatment with too low a dose or for too brief a period is undoubtedly the main cause of the rare relapses that occur in adults. When a large volume of brain tissue is involved, the hemorrhagic necrosis and surrounding edema act as an enlarging mass that requires separate attention. There is increased signal from practically all of the inferior and deep temporal lobe and the insular cortex. Right: a T1-weighted image after gadolinium infusion showing enchancement of the left insular and temporal cortices and early involvement of the right temporal lobe. All measures used in the management of brain edema due to mass lesions should be applied, but there are insufficient data by which to judge their effectiveness. The concern that corticosteroids may aggravate the infection has not been borne out by clinical experience, but a detrimental effect cannot be discounted. Our experience (reported by Barnett et al) and that of Schwab and colleagues has been that the presence of raised intracranial pressure early in the illness presages a poor outcome. Seizures are usually brought under control by high doses of conventional anticonvulsants. If the patient is unconscious (except immediately after a convulsion), the outcome is uniformly poor. However, if treatment is begun within 4 days of onset of the illness in an awake patient, survival is greater than 90 percent (Whitley). Evaluation of these patients 2 years after treatment showed 38 percent to be normal or nearly normal, whereas 53 percent were dead or severely impaired. The neurologic sequelae are often of the most serious type, consisting of a Korsakoff amnesic defect or a global dementia, seizures, and aphasia (Drachman and Adams). With the exception of the aforementioned rare relapsing cases, the infection does not recur. As indicated in the introductory section, the virus spreads along peripheral nerves to reach the nervous system. Rare cases have been caused by inhalation of the virus shed by bats; in a few cases the source of the infection may not be identifiable. The epidemiology and public health aspects of rabies have been reviewed by Fishbein and Robinson. Clinical Features the incubation period is usually 20 to 60 days but may be as short as 14 days, especially in cases involving multiple deep bites around the face and neck. Tingling or numbness at the site of the bite, even after the wound has healed, is characteristic. This is thought to reflect an inflammatory response that is incited when the virus reaches the sensory ganglion. The main neurologic symptoms (following a 2- to 4-day prodromal period of fever, headache, and malaise) consist of severe apprehension, dysarthria, and psychomotor overactivity, followed by dysphagia (hence salivation and "frothing at the mouth"), spasms of throat muscles induced by attempts to swallow water or in rare cases by the mere sight of water (hence "hydrophobia"), dysarthria, numbness of the face, and spasms of facial muscles. This localization indicates the involvement of the tegmental medullary nuclei in the rabid form of the disease. A less common paralytic form ("dumb" rabies of older writings, in distinction to the above described "furious" form) due to spinal cord infection, may accompany or replace the state of excitement. The paralytic form is most likely to follow bat bites or, in the past, the administration of rabies vaccination. Coma gradually follows the acute encephalitic symptoms and death ensues within 4 to 10 days, or longer in the paralytic form. In addition to mechanical respiratory support, several secondary abnormalities must be addressed, including raised intracranial pressure, excessive release of antidiuretic hormone, diabetes insipidus, and extremes of autonomic dysfunction, especially hyper- and hypotension. Pathologic Features the disease is distinguished by the presence of cytoplasmic eosinophilic inclusions, the Negri bodies. In addition there may be widespread perivascular cuffing and meningeal infiltration with lymphocytes and mononuclear cells and small foci of inflammatory necrosis, such as those seen in other viral infections. The focal collections of microglia in this disease are referred to as Babes nodules (named for Victor Babes, a Romanian microbiologist). Treatment Bites and scratches from a potentially rabid animal should be thoroughly washed with soap and water and, after all soap has been removed, cleansed with benzyl ammonium chloride (Zephiran), which has been shown to inactivate the virus. After a bite by a seemingly healthy animal, surveillance of the animal for a 10-day period is necessary. Should signs of illness appear in the animal, it should be killed and the brain sent, under refrigeration, to a government-designated laboratory for appropriate diagnostic tests. Wild animals, if captured, should be killed and the brain examined in the same way. If the animal is found by fluorescent antibody or other tests to be rabid or if the patient was bitten by a wild animal that escaped, Rabies this disease also stands apart from other acute viral infections by virtue of the latent period that follows inoculation with the virus and its distinctive clinical and pathologic features. Human examples of this disease are rare in the United States; between 1980 and 1997, only 34 such cases are known to have occurred; since 1960, there have never been more than 5 or so cases in any one year. In some areas (Australia, Hawaii, Great Britain, and the Scandinavian peninsula), no indigenous cases have ever been reported; in India, however, there is a high incidence. The importance of this disease derives from two facts: it has been almost invariably fatal once the characteristic clinical features appear; hence the survival of the infected individual depends upon the institution of specific therapeutic measures before the infection becomes clinically evident. Furthermore, each year 20,000 to 30,000 individuals are treated with rabies vaccine, having been bitten by animals that possibly were rabid, and although the incidence of complications with the newer rabies vaccination is much lower than before, a few serious reactions continue to be encountered (see below and also Chap. Etiology Practically all cases of rabies are the result of transdermal viral inoculation by an animal bite. In undeveloped countries, where rabies is relatively common, the most frequent source is the rabid dog. In western Europe and the United States, the most common rabid species are raccoons, skunks, foxes, and bats among wild animals and dogs and cats among domestic ones. Because rabid animals commonly bite without provocation, the nature of the attack should be determined. This provides passive immunization for 10 to 20 days, allowing time for active immunization. A thorough trial of the new antiviral agents in patients already symptomatic has not been undertaken. Syndromes of Herpes Zoster Herpes zoster ("shingles," "zona") is a common viral infection of the nervous system occurring at an overall rate of 3 to 5 cases per 1000 persons per year, with higher rates in the elderly. It is characterized clinically by radicular pain, a vesicular cutaneous eruption, and, less often, by segmental sensory and delayed motor loss. The pathologic changes consist of an acute inflammatory reaction in isolated spinal or cranial sensory ganglia and lesser degrees of reaction in the posterior and anterior roots, the posterior gray matter of the spinal cord, and the adjacent leptomeninges. The neurologic implications of the segmental distribution of the rash were recognized by Richard Bright as long ago as 1831. Inflammatory changes in the corresponding ganglia and related portions of the spinal nerves were first described by von Barensprung in 1862 and were later studied extensively. The concept that varicella and zoster are caused by the same agent was introduced by von Bokay in 1909 and was subsequently established by Weller and his associates (1954, 1958). These and other historical features of herpes zoster have been reviewed by DennyBrown and Adams and by Weller and their colleagues. This hypothesis is consistent with the differences in the clinical manifestations of chickenpox and herpes zoster, even though both are caused by the same virus. Chickenpox is highly contagious by respiratory aerosol, has a well-marked seasonal incidence (winter and spring), and tends to occur in epidemics. Zoster, on the other hand, is not communicable (except to a person who has not had chickenpox), occurs sporadically throughout the year, and shows no increase in incidence during epidemics of chickenpox. In patients with zoster, there is practically always a past history of chickenpox. The supposition is that in both zoster and varicella infections the virus makes its way from the cutaneous Acute Cerebellitis (Acute Ataxia of Childhood) A special comment should be made here concerning the dramatic syndrome of acute ataxia that occurs in the context of an infectious illness. The syndrome was originally described by Westphal in 1872 following smallpox and typhoid fever in adults, but Batten is credited with drawing attention to the more common ataxic illness that occurs after certain childhood infections such as measles, pertussis, and scarlet fever. The syndrome, which is essentially a "meningocerebellitis," appears relatively abruptly, over a day or so, and consists of limb and gait ataxia and often dysarthria and nystagmus. The fever of the original infection may have abated, or it may persist through the early stages of the ataxic illness. Because the benign nature of the illness has precluded extensive pathologic study, there is still uncertainty regarding the infectious or postinfectious nature of these ataxic illnesses. Some cases have shown an inflammatory pathology most suggestive of a postinfectious process (see Chap. Multiplication of the virus in epidermal cells causes swelling, vacuolization, and lysis of cell boundaries, leading to the formation of vesicles and so-called Lipschutz inclusion bodies. Alternatively, the ganglia could be infected during the viremia of chickenpox, but then one would have to explain why only one or a few sensory ganglia become infected. Clinical Features As indicated above, the incidence of herpes zoster rises with age. Hope-Simpson has estimated that if a cohort of 1000 people lived to 85 years of age, half would have had one attack of zoster and 10 would have had two attacks. Herpes zoster occurs in up to 10 percent of patients with lymphoma and 25 percent of patients with Hodgkin disease- particularly in those who have undergone splenectomy or received radiotherapy. Conversely, about 5 percent of patients who present with herpes zoster are found to have a concurrent malignancy (about twice the number that would be expected), and the proportion appears to be even higher if more than two adjacent dermatomes are involved. The vesicular eruption is usually preceded for several days by itching, tingling, or burning sensations in the involved dermatome(s), and sometimes by malaise and fever as well. Or there is severe localized or radicular pain that may be mistaken for pleurisy, appendicitis, cholecystitis, or, quite often, ruptured intervertebral disc, until the diagnosis is clarified by the appearance of vesicles (nearly always within 72 to 96 h). The rash consists of clusters of tense clear vesicles on an erythematous base, which become cloudy after a few days (due to accumulation of inflammatory cells) and dry, crusted, and scaly after 5 to 10 days. In a small number of patients, the vesicles are confluent and hemorrhagic, and healing is delayed for several weeks. In most cases pain and dysesthesia last for 1 to 4 weeks; but in the others (7 to 33 percent in different series) the pain persists for months or, in different forms, even for years and presents a difficult problem in management. Impairment of superficial sensation in the affected dermatome(s) is common, and segmental weakness and atrophy are added in about 5 percent of patients. In the majority of patients the rash and sensorimotor signs are limited to the territory of a single dermatome, but in some, particularly those with cranial or limb involvement, two or more contiguous dermatomes are involved. Rarely (and usually in association with malignancy) the rash is generalized, like that of chickenpox, or altogether absent. ЁЁ Virtually any dermatome may be involved in zoster, but some regions are far more frequent than others. The thoracic dermatomes, particularly T5 to T10, are the most common sites, accounting for more than two-thirds of all cases, followed by the craniocervical regions. In the latter cases the disease tends to be more severe, with greater pain, more frequent meningeal signs, and involvement of the mucous membranes. There are two rather characteristic cranial herpetic syndromes- ophthalmic herpes and so-called geniculate herpes. In ophthalmic herpes, which accounts for 10 to 15 percent of all cases of zoster, the pain and rash are in the distribution of the first division of the trigeminal nerve, and the pathologic changes are centered in the gasserian ganglion. The main hazard in this form of the disease is herpetic involvement of the cornea and conjunctiva, resulting in corneal anesthesia and residual scarring. Palsies of extraocular muscles, ptosis, and mydriasis are frequently associated, indicating that the third, fourth, and sixth cranial nerves are affected in addition to the gasserian ganglion. A less common but also characteristic cranial nerve syndrome consists of a facial palsy in combination with a herpetic eruption of the external auditory meatus, sometimes with tinnitus, vertigo, and deafness. Ramsay Hunt (whose name has been attached to the syndrome) attributed this syndrome to herpes of the geniculate ganglion. Denny-Brown and Adams found the geniculate ganglion to be only slightly affected in a man who died 64 days after the onset of a so-called Ramsay Hunt syndrome (during which time the patient had recovered from the facial palsy); there was, however, inflammation of the facial nerve. Herpes zoster of the palate, pharynx, neck, and retroauricular region (herpes occipitocollaris) depends on herpetic infection of the upper cervical roots and the ganglia of the vagus and glossopharyngeal nerves. Herpes zoster in this distribution may also be associated with the Ramsay Hunt syndrome. Encephalitis and cerebral angiitis are rare but well-described complications of cervicocranial zoster, as discussed below, and a restricted but destructive myelitis is a similarly rare but often quite serious complication of thoracic zoster. Devinsky and colleagues reported their findings in 13 patients with zoster myelitis (all of them immunocompromised) and reviewed the literature on this subject. The signs of spinal cord involvement appeared 5 to 21 days after the rash and then progressed for a similar period of time. Asymmetrical paraparesis and sensory loss, sphincteric disturbances, and, less often, a Brown-Sequard syndrome were the usual ґ clinical manifestations. The pathologic changes, which take the form of a necrotizing inflammatory myelopathy and vasculitis, involve not just the dorsal horn but also the contiguous white matter, predominantly on the same side and at the same segment(s) as the affected dorsal roots, ganglia, and posterior horns. Our experience with the problem includes an elderly man who was not immunosuppressed; he remained with an almost complete transverse myelopathy. Many of the writings on zoster encephalitis give the impression of a severe illness that occurs temporally remote from the attack of shingles in an immunosuppressed patient. However, our experience is more in keeping with that of Jemsek and colleagues and of Peterslund, who described a less severe form of encephalitis in patients with normal immune systems. Several of our patients, all elderly women, developed self-limited encephalitis during the latter stages of an attack of shingles. They were confused and drowsy, with low-grade fever but little meningismus, and a few had seizures. The differential diagnosis in these elderly patients also includes a drowsy-confusional state induced by narcotics given for the control of pain. Angiograms show narrowing or occlusion of the internal carotid artery adjacent to the ganglia; but in some cases, vasculitis is more diffuse, even involving the contralateral hemisphere. Whether the angiitis results from direct spread of the viral infection via neighboring nerves as postulated by Linnemann and Alvira or represents an allergic reaction during convalescence from zoster has not been settled. Since the exact pathogenetic mechanism is uncertain, treatment with both intravenous acyclovir and corticosteroids may be justified. In this condition, weeks or months after one or more attacks of zoster, a subacute encephalitis ensues, including fever and focal signs. The vasculitic and other neurologic complications of zoster have been reviewed by Gilden and colleagues. Finally, it must be conceded that a facial palsy or pain in the distribution of a trigeminal or segmental nerve (usually lumbar or intercostal) due to herpetic ganglionitis, may occur very rarely without involvement of the skin (zoster sine herpete); lumbar disc herniation may be suspected. Treatment During the acute stage, analgesics and drying and soothing lotions, such as calamine, help to blunt the pain. After the lesions have dried, the repeated application of capsaicin ointment (derived from hot peppers) may relieve the pain in some cases by inducing a cutaneous anesthesia. When applied too soon after the acute stage, capsaicin is highly irritating and should be used cautiously. Acyclovir (800 mg orally five times daily for 7 days) shortens the duration of acute pain and speeds the healing of vesicles, provided that treatment is begun within approximately 48 h (some authorities say 72 h) of the appearance of the rash (McKendrick et al).
This may be followed by generalized seizures in the first 2448 h; these do not require initiation of antiseizure medications silent treatment cheap 16mg betahistine with amex. How often during the last year have you found that you were not able to stop drinking once you had started? How often during the last year have you failed to do what was normally expected from you because of drinking? How often during the last year have you needed a first drink in the morning to get yourself going after a heavy drinking session? How often during the last year have you had a feeling of guilt or remorse after drinking? How often during the last year have you been unable to remember what happened the night before because you had been drinking? Has a relative medications not covered by medicare buy generic betahistine 16mg, friend medications like prozac buy betahistine 16mg without prescription, doctor or other health worker been concerned about your drinking or suggested that you should cut down? Risks include overmedication and oversedation medicine 219 cheap betahistine 16 mg line, which occur less commonly with shorter-acting agents medicine joint pain buy 16 mg betahistine mastercard. Generalized withdrawal seizures rarely require aggressive pharmacologic intervention beyond that given to the usual pt undergoing withdrawal treatment lower back pain generic 16mg betahistine fast delivery, i symptoms appendicitis betahistine 16 mg with mastercard. A third component symptoms xanax withdrawal purchase betahistine 16 mg on-line, called relapse prevention, helps the person to identify situations in which a return to drinking is likely, formulate ways of managing these risks, and develop coping strategies that increase the chances of a return to abstinence if a slip occurs. There is no convincing evidence that inpatient rehabilitation is more effective than outpatient care. Drug Therapy Several medications may be useful in alcoholic rehabilitation; usually medications are continued for 612 months if a positive response is seen. These receptors mediate the opiate effects of analgesia, euphoria, respiratory depression, and constipation. Endogenous opiate peptides (enkephalins and endorphins) are natural ligands for the opioid receptors and play a role in analgesia, memory, learning, reward, mood regulation, and stress tolerance. The prototypic opiates, morphine and codeine, are derived from the juice of the opium poppy, Papaver somniferum. Pts with chronic pain syndromes who misuse their prescribed analgesics · Physicians, nurses, dentists, and pharmacists with easy access to narcotics · "Street" abusers. In larger doses, markedly decreased respirations, bradycardia, pupillary miosis, stupor, and coma ensue. Additionally, the adulterants used to "cut" street drugs (quinine, phenacetin, strychnine, antipyrine, caffeine, powdered milk) can produce permanent neurologic damage, including peripheral neuropathy, amblyopia, myelopathy, and leukoencephalopathy; adulterants can also produce an "allergic-like" reaction characterized by decreased alertness, frothy pulmonary edema, and an elevation in blood eosinophil count. Chronic Effects Chronic use of opiates will result in tolerance (requiring higher doses to achieve psychotropic effects) and physical dependence. Withdrawal Withdrawal produces nausea and diarrhea, coughing, lacrimation, mydriasis, rhinorrhea, diaphoresis, twitching muscles, piloerection, fever, tachypnea, hypertension, diffuse body pain, insomnia, and yawning. With longer-acting opiates such as methadone, withdrawal begins several days after the last dose, peaks at 710 days in some cases, and lasts several weeks. Narcotic Abuse Overdose High doses of opiates, whether taken in a suicide attempt or accidentally when its potency is misjudged, are potentially lethal. Symptoms include miosis, shallow respirations, bradycardia, hypothermia, and stupor or coma. Treatment requires cardiorespiratory support, using intubation if needed, and administration of the opiate antagonist naloxone (0. Because the effects of naloxone diminish in 23 h compared with longer-lasting effects of heroin (up to 24 h) or methadone (up to 72 h), pts must be observed for at least 13 days for reappearance of the toxic state. Withdrawal One treatment approach to withdrawal is the administration of any opioid. Comfort can be enhanced with administration of the 2-adrenergic agonist clonidine in doses up to 0. Some clinicians augment this regimen with low to moderate doses of benzodiazepines for 25 days to decrease agitation. An ultrarapid detoxification procedure using deep sedation and withdrawal precipitated by naltrexone has many inherent dangers and few, if any, advantages. Opioid Maintenance Methadone maintenance is a widely used treatment strategy in the management of opiate addiction. Methadone is a long-acting opioid optimally dosed at 80120 mg/d (gradually increased over time). This level is optimally effective in blocking heroin-induced euphoria, decreasing craving, and maintaining abstinence from illegal opioids. Over three-quarters of patients in wellsupervised methadone clinics are likely to remain heroin-free for 6 months. An additional medication that has been used for maintenance treatment involves the opioid agonist and antagonist buprenorphine; it has several advantages, including low overdose danger, potentially easier detoxification than with methadone, and a probable ceiling effect in which higher doses do not increase euphoria. Drug-Free Programs Most opioid treatment programs focus primarily on cognitive-behavioral approaches of enhancing commitment to abstinence, helping individuals to rebuild their lives without substances, and preventing relapse. Whether carried out in inpatient or outpatient settings, patients do not receive maintenance medications. Physicians must be vigilant regarding their own risk for opioid abuse and dependence, never prescribing these drugs for themselves. For the nonmedical intravenous drugdependent person, all possible efforts must be made to prevent the infectious consequences of contaminated needles both through methadone maintenance and by considering needle-exchange programs. Several measurements have been derived to better assess the potential gain from screening and prevention interventions: · Number of subjects needed to be screened to alter the outcome in one individual · Absolute impact of screening on disease. History should include medication use, allergies, dietary history, use of alcohol and tobacco, sexual practices, safety practices (seat belt and helmet use, gun possession), and a thorough family history. Tobacco and alcohol use, diet, and exercise represent the vast majority of factors that influence preventable deaths. While behavioral changes are frequently difficult to achieve, it should be emphasized that studies show even brief (<5 min) tobacco counseling by physicians results in a significant rate of long-term smoking cessation. The top causes of age-specific mortality and corresponding preventative strategies are listed in Table 211-1. Specific recommendations for disease prevention can also be found in subsequent chapters on Immunization and Advice to Travelers (Chap. Products used for this purpose are standard human immune serum globulin, special immune serum globulins with a known content of antibody to specific agents. However, travelers should be certain that their routine immunizations are up to date because certain diseases. After the birth dose: the HepB series should be completed with either monovalent HepB or a combination vaccine containing HepB. If monovalent HepB is used for doses after the birth dose, a dose at age 4 months is not needed. All children aged 659 months and close contacts of all children aged 059 months are recommended to receive influenza vaccine. Influenza vaccine is recommended annually for children aged 59 months with certain risk factors, health-care workers, and other persons (including household members) in close contact with persons in groups at high risk. Varicella vaccine may be administered before age 46 years, provided that 3 months have elapsed since the first dose and both doses are administered at age 12 months. If the second dose was administered 28 days following the first dose, the second dose does not need to be repeated. Children not fully vaccinated by age 2 years can be vaccinated at subsequent visits. HepA is recommended for certain other groups of children, including in areas where vaccination programs target older children. Administer the second dose 2 months after the first dose and the third dose 6 months after the first dose. Vaccination against invasive meningococcal disease is recommended for children and adolescents aged 2 years with terminal complement deficiencies or anatomic or functional asplenia and certain other high-risk groups. Influenza vaccine is recommended annually for persons with certain risk factors, health-care workers, and other persons (including household members) in close contact with persons in groups at high risk. Administer 2 doses of varicella vaccine to persons aged <13 years at least 3 months apart. Administer 2 doses of varicella vaccine to persons aged 13 years at least 4 weeks apart. This schedule indicates the recommended age groups for routine administration of currently licensed vaccines for persons aged 19 years, as of October 1, 2006. Information on how to file a Vaccine Injury Compensation Program claim is available at. Additional information about the vaccines in this schedule and contraindications for vaccination is also available at. Adults with uncertain histories of a complete primary vaccination series with diphtheria and tetanus toxoidcontaining vaccines should begin or complete a primary vaccination series. A primary series for adults is 3 doses; administer the first 2 doses at least 4 weeks apart and the third dose 612 months after the second. Administer a booster dose to adults who have completed a primary series and if the last vaccination was received 10 years previously. Tdap or tetanus and diphtheria (Td) vaccine may be used; Tdap should replace a single dose of Td for adults aged <65 years who have not previously received a dose of Tdap (either in the primary series, as a booster, or for wound management). Only one of two Tdap products (Adacel [sanofi pasteur]) is licensed for use in adults. If the person is pregnant and received the last Td vaccination 10 years previously, administer Td during the second or third trimester; if the person received the last Td vaccination in <10 years, administer Tdap during the immediate postpartum period. A one-time administration of 1 dose of Tdap with an interval as short as 2 years from a previous Td vaccination is recommended for postpartum women, close contacts of infants aged <12 months, and all healthcare workers with direct patient contact. In certain situations, Td can be deferred during pregnancy and Tdap substituted in the immediate postpartum period, or Tdap can be given instead of Td to a pregnant woman after an informed discussion with the woman (see The second dose should be administered 2 months after the first dose; the third dose should be administered 6 months after the first dose. If a woman is found to be pregnant after initiating the vaccination series, the remainder of the 3-dose regimen should be delayed until after completion of the pregnancy. For unvaccinated healthcare workers born before 1957 who do not have other evidence of mumps immunity, consider giving 1 dose on a routine basis and strongly consider giving a second dose during an outbreak. For women of childbearing age, regardless of birth year, routinely determine rubella immunity and counsel women regarding congenital rubella syndrome. Do not vaccinate women who are pregnant or who might become pregnant within 4 weeks of receiving vaccine. All adults without evidence of immunity to varicella should receive 2 doses of varicella vaccine. Special consideration should be given to those who (1) have close contact with persons at high risk for severe disease. Evidence of immunity to varicella in adults includes any of the following: (1) documentation of 2 doses of varicella vaccine at least 4 weeks apart; (2) U. Do not vaccinate women who are pregnant or might become pregnant within 4 weeks of receiving the vaccine. Women who do not have evidence of immunity should receive dose 1 of varicella vaccine upon completion or termination of pregnancy and before discharge from the healthcare facility. No data exist on the risk for severe or complicated influenza disease among persons with asplenia; however, influenza is a risk factor for secondary bacterial infections that can cause severe disease among persons with asplenia. Occupational indications: healthcare workers and employees of long-termcare and assisted living facilities. Other indications: residents of nursing homes and other long-termcare and assisted living facilities; persons likely to transmit influenza to persons at high risk. Healthy, nonpregnant persons aged 549 years without high-risk medical conditions who are not contacts of severely immunocompromised persons in special care units can receive either intranasally administered influenza vaccine (FluMist) or inactivated vaccine. Medical indications: chronic disorders of the pulmonary system (excluding asthma); cardiovascular diseases; diabetes mellitus; chronic liver diseases, including liver disease as a result of alcohol abuse. Other indications: Alaska Natives and certain American Indian populations and residents of nursing homes or other long-termcare facilities. One-time revaccination after 5 years for persons with chronic renal failure or nephrotic syndrome; functional or anatomic asplenia. For persons aged 65 years, one-time revaccination if they were vaccinated 5 years previously and were aged <65 years at the time of primary vaccination. Medical indications: persons with chronic liver disease and persons who receive clotting factor concentrates. Behavioral indications: men who have sex with men and persons who use illegal drugs. Other indications: persons traveling to or working in countries that have high or intermediate endemicity of hepatitis A (a list of countries is available at Current vaccines should be administered in a 2-dose schedule at either 0 and 612 months, or 0 and 618 months. If the combined hepatitis A and hepatitis B vaccine is used, administer 3 doses at 0, 1, and 6 months. Occupational indications: healthcare workers and public-safety workers who are exposed to blood or other potentially infectious body fluids. Behavioral indications: sexually active persons who are not in a long-term, mutually monogamous relationship. Medical indications: adults with anatomic or functional asplenia, or terminal complement component deficiencies. Other indications: first-year college students living in dormitories; microbiologists who are routinely exposed to isolates of Neisseria meningitidis; military recruits; and persons who travel to or live in countries in which meningococcal disease is hyperendemic or epidemic. Vaccination is required by the government of Saudi Arabia for all travelers to Mecca during the annual Hajj. In addition, personal protective measures against mosquito bites, especially between dusk and dawn. The incidence is highest in parts of Africa, Central and South America, and Southeast Asia. Although self-limited, diarrheal illness alters travel plans and confines 20% of pts to bed. Moderate to severe diarrhea should be treated with a 3-day course or a single double dose of a fluoroquinolone. High rates of quinolone-resistant Campylobacter in Thailand make azithromycin a better choice for that country. Rifaximin, a poorly absorbed rifampin derivative, is highly effective against noninvasive bacterial pathogens such as toxigenic and enteroaggregative E. Relative contraindications to international travel during pregnancy include a history of miscarriage, premature labor, incompetent cervix, or toxemia or the presence of other general medical problems. Malaria is acquired most often in Africa, dengue in Southeast Asia and the Caribbean, typhoid fever in southern Asia, and rickettsial infections in southern Africa. Identification and control of these attributes reduce subsequent cardiovascular event rates. Observational studies show that smoking cessation reduces excess risk of coronary events within months; after 35 years, the risk falls to that of individuals who never smoked. Patients should be asked regularly about tobacco use, followed by counseling and, as needed, antismoking pharmacologic therapy to assist cessation. Cardiovascular event rates in elderly patients with isolated systolic hypertension (systolic > 160 but diastolic < 90) are also reduced by antihypertensive therapy. Dietary counseling, weight loss, and increased physical activity are important in reducing the prevalence of this syndrome. Male Gender/Postmenopausal State Coronary risk is greater in men compared to that of premenopausal women of same age, but female risk accelerates after menopause. However, prospective clinical trials do not support such a benefit and hormone-replacement therapy should not be prescribed for the purpose of cardiovascular risk reduction, especially in older women. Homocysteine There is a graded correlation between serum homocysteine levels and risk of cardiovascular events and stroke. Supplemental folic acid and other B vitamins lower serum levels, but prospective clinical trials have not shown that such therapy reduces cardiac events. The American Heart Association recommends aspirin (75160 mg daily) for men and women who are at high cardiovascular risk. For a more detailed discussion, see Libby P: the Pathogenesis, Prevention, and Treatment of Atherosclerosis, Chap. Every physician visit is an opportunity to teach and reinforce the elements of a healthy lifestyle. Cancer screening in the asymptomatic population at average risk is a complicated issue. To be of value, screening must detect disease at a stage that is more readily curable than disease that is treated after symptoms appear. Screening can cause harm; complications may ensue from the screening test or the tests done to validate a positive screening test or from treatments for the underlying disease. Lead-time bias occurs when the natural history of disease is unaffected by the diagnosis, but the pt is diagnosed earlier in the course of disease than normal; thus, the pt spends more of his/her life span knowing the diagnosis. Length bias occurs when slow-growing cancers that might never have come to medical attention are detected during screening. Selection bias is the term for the fact that people who volunteer for screening trials may be different from the general population. The various groups that evaluate and recommend screening practice guidelines have used varying criteria to make their recommendations (Table 214-2). One study shows some advantage for women who are screened starting at age 40 that appears 15 years later; however, it is unclear if this benefit would not have also been derived by starting screening at age 50 years. Women age 4049 years have a much lower incidence of breast cancer and a higher false-positive rate on mammography. Nearly half of women screened during their forties will have a false-positive test. However, colonoscopy is the gold standard in colorectal cancer detection, but it is expensive and has not been shown to be cost-effective in asymptomatic people.
Caplan has summarized the features of other mixed oculomotor defects that occur with thrombotic occlusion of the upper part of the basilar artery ("top of the basilar" syndromes) medicine used during the civil war generic 16mg betahistine free shipping. These include upgaze or complete vertical gaze palsy and so-called pseudoabducens palsy medicine vs dentistry cheap 16 mg betahistine overnight delivery, mentioned earlier symptoms 8 days before period quality betahistine 16 mg. The latter is characterized by bilateral incomplete esotropia that simulates bilateral sixth nerve paresis but appears to be a type of sustained convergence or a paresis of divergence; it can be overcome by vestibular stimulation medicine evolution betahistine 16mg amex. Among the most unusual of the complex ocular disturbances is a subjective tilting of the entire visual field that may produce any angle of divergence but most often creates an illusion of tilting of 45 to 90 degrees (tortopia) or of 180-degree vision (upside-down vision) medicine expiration dates discount 16 mg betahistine with amex. Objects normally on the floor treatment tinea versicolor purchase betahistine 16 mg without prescription, such as chairs and tables treatment 8th march buy 16 mg betahistine fast delivery, are perceived to be on the wall or ceiling symptoms you are pregnant generic 16 mg betahistine. Lateral medullary infarction has been the most common cause in our experience (Ropper). The observation of suppression with visual fixation is facilitated by the use of Frenzel lenses, but most instances are evident without elaborate apparatus. In contrast, as noted below, nystagmus of brainstem and cerebellar origin is most apparent when the patient fixates upon and follows a moving target and the direction of nystagmus changes with the direction of gaze as noted below and discussed in Chap. Labyrinthine-vestibular nystagmus may be horizontal, vertical, or oblique, and that of purely labyrinthine origin characteristically has an additional torsional component. Tinnitus and hearing loss are often associated with disease of the peripheral labyrinthine mechanism; also, vertigo, nausea, vomiting, and staggering may accompany disease of any part of the labyrinthine-vestibular apparatus or its central connections. As a characteristic example, the intense nystagmus or benign positional vertigo (described fully on page 261) is evoked by the action of moving from the sitting to the supine position, or the opposite, with the head turned to one side. In this condition, nystagmus of vertical-torsional type and vertigo develop in a few seconds and persist for another 10 to 15 s. When the patient sits up quickly, the nystagmus changes to beat in the opposite direction. In many normal individuals, a few irregular jerks of the eyes are observed when the eyes are moved far to one side ("nystagmoid" jerks), but the movements cease once lateral fixation is attained. A fine rhythmic nystagmus may also occur in extreme lateral gaze, beyond the range of binocular vision; but if it is bilateral and disappears as the eyes move a few degrees toward the midline, it usually has no clinical significance. These movements are probably analogous to the tremulousness of skeletal muscles when maximally contracted. Nystagmus Due to Brainstem and Cerebellar Disease Brainstem lesions often cause a coarse, unidirectional, gaze-dependent nystagmus, which may be horizontal or vertical, meaning that the nystagmus is exaggerated when the eyes sustain an eccentric position of gaze; vertical nystagmus, for example, is brought out usually on upward gaze, less often on downward gaze. Unlike the vestibular nystagmus discussed above, the central type usually changes direction depending on the direction of gaze. The presence of bidirectional vertical nystagmus usually indicates disease in the pontomedullary or mesencephalic tegmentum. Vertigo is less common or less intense than with labyrinthine nystagmus, but signs of disease of other nuclear structures and tracts in the brainstem are frequent. Upbeat nystagmus is observed frequently in patients with demyelinative or vascular disease, tumors, or Wernicke disease. According to some authors, it has been associated with lesions of the anterior cerebellar vermis, but we have not observed such an association. Kato and associates cite cases with a lesion at the pontomedullary junction, involving the nucleus prepositus hypoglossi, which receives vestibular connections and projects to all Nystagmus Nystagmus refers to involuntary rhythmic movements of the eyes and is of two general types. In the more common jerk nystagmus, the movements alternate between a slow component and a fast corrective component, or jerk, in the opposite direction. In pendular nystagmus, the oscillations are roughly equal in rate in both directions, although on lateral gaze the pendular type may be converted to the jerk type, with the fast component to the side of gaze. Nystagmus reflects an imbalance in one or more of the systems that maintain stability of gaze. For the purposes of clinical work, however, certain types of nystagmus are identified as corresponding to lesions in specific structures within each of these systems, and it is this approach that we take in the following pages. In testing for nystagmus, the eyes should be examined first in the central position and then during upward, downward, and lateral movements. It may be horizontal or vertical and is elicited particularly on ocular movement in these planes, or it may be rotatory and, rarely, retractory or vergent. By custom the direction of the nystagmus is named according to the direction of the fast component. Some occur spontaneously; others are readily induced in normal persons by drugs or by labyrinthine or visual stimulation. Alcohol, barbiturates, other sedative-hypnotic drugs, and phenytoin are the common ones. This form of nystagmus is most prominent on deviation of the eyes in the horizontal plane, but occasionally it may appear in the vertical plane as well. It rarely appears in the vertical plane alone, suggesting then a tegmental brainstem disorder or lithium intoxication. Oscillopsia is the illusory movement of the environment in which stationary objects seem to move back and forth, up and down, or from side to side. With lesions of the labyrinths (as in aminoglycoside toxicity), oscillopsia is characteristically provoked by motion-. Downbeat nystagmus, which is always of central origin, is characteristic of lesions in the medullary-cervical region such as syringobulbia, Chiari malformation, basilar invagination, and demyelinative plaques. It has also been seen with Wernicke disease and may be an initial sign of either paraneoplastic brainstem encephalitis or cerebellar degeneration with opsoclonus. Downbeat nystagmus, usually in association with oscillopsia, has also been observed in patients with lithium intoxication or with profound magnesium depletion (Saul and Selhorst). Halmagyi and coworkers, who studied 62 patients with downbeat nystagmus, found that in half of them this abnormality was associated with the Chiari malformation and various forms of cerebellar degeneration; in most of the remainder, the cause could not be determined. However, a large proportion of cases of downbeating nystagmus remain unexplained by any of these mechanisms. Nystagmus of several types- including gaze-evoked nystagmus, downbeat nystagmus, and "rebound nystagmus" (gazeevoked nystagmus that changes direction with refixation to the primary position)- occurs with cerebellar disease (more specifically with lesions of the vestibulocerebellum) or with brainstem lesions that involve the nucleus prepositus hypoglossi and the medial vestibular nucleus (see above, in relation to upbeat nystagmus). Characteristic of cerebellar disease are several closely related disorders of saccadic movement (opsoclonus, flutter, dysmetria) described below. Tumors situated in the cerebellopontine angle may cause a coarse bilateral horizontal nystagmus, coarser to the side of the lesion. Nystagmus that occurs only in the abducting eye is referred to as dissociated nystagmus and is a common sign of internuclear ophthalmoplegia, as discussed above. Pendular Nystagmus this is found in a variety of conditions in which central vision is lost early in life, such as albinism and various other diseases of the retina and refractive media (congenital ocular nystagmus). Occasionally it is observed as a congenital abnormality, even without poor vision. The defect is postulated to be an instability of smooth pursuit or gaze-holding mechanisms. It is purely or mainly pendular (sinusoidal) except in extremes of gaze, when it comes to resemble jerk nystagmus. The oscillations of the eyes are usually very rapid, increase on upward gaze, and may be associated with compensatory oscillations of the head and intolerance of light. Indications as to the congenital nature of nystagmus are that it remains horizontal in all directions of gaze; it is suppressed during convergence and may be associated with odd head positions or with head oscillations and with strabismus. Also characteristic is a paradoxical response to optokinetic testing (see below), in which the quick phase is in the same direction as the drum rotation. A related latent nystagmus is the result of a lack of normal development of stereoscopic vision and may be detected by noting that the nystagmus changes direction when the eyes are alternately covered. In addition, severe visual loss or blindness of acquired type that eliminates the ability to accurately direct gaze, even in adulthood, produces nystagmus of pendular or jerk variety. Both horizontal and vertical components are evident and the characteristic feature is a fluctuation over several seconds of observation in the dominant direction of beating. Spasmus mutans, a specific type of pendular nystagmus of infancy, is accompanied by head nodding and occasionally by wry positions of the neck. Most cases begin between the fourth and twelfth months of life, never after the third year. The nystagmus may be horizontal, vertical, or rotatory; it is usually more pronounced in one eye than the other (or limited to one eye) and can be intensified by immobilizing or straightening the head. Most cases are idiopathic, but symptoms like those of spasmus mutans betray the presence of a chiasmal or third ventricular tumor (see also seesaw nystagmus below). The explanation of this phenomenon is that the slow component of the nystagmus represents an involuntary pursuit movement to the limit of comfortable conjugate gaze; the eyes then make a quick saccadic movement in the opposite direction in order to fixate a new target that is entering the visual field. These observations indicate that an abnormal response does not depend on a lesion of the geniculocalcarine tract. Presumably the loss of the pursuit phase with a parietal lesion is due to interruption of efferent pathways from the parietal cortex to the brainstem centers for conjugate gaze. On the other hand, frontal lobe lesions allow the eyes to tonically follow in the direction of the target but with little or no fast-phase correction in the direction opposite the lesion. Cold water induces a slow tonic deviation of the eyes toward the ear irrigated by a cold stimulus and a compensatory nystagmus in the opposite direction; warm water does the reverse. The production of nystagmus by labyrinthine stimulation and other features of vestibular nystagmus are discussed further in Chap. Other Types of Nystagmus Convergence nystagmus refers to a rhythmic oscillation in which a slow abduction of the eyes in respect to each other is followed by a quick movement of adduction. It is usually accompanied by quick rhythmic retraction movements of the eyes (nystagmus retractorius) and by one or more features of the Parinaud dorsal midbrain syndrome. These unusual phenomena all point to a lesion of the upper midbrain tegmentum and are usually manifestations of vascular disease, traumatic disease, or tumor, notably pinealoma that compresses this region. Seesaw nystagmus is a torsional-vertical oscillation in which the intorting eye moves up and the opposite (extorting) eye moves down, then both move in the reverse direction. It is occasionally observed in conjunction with chiasmatic bitemporal hemianopia due to sellar or parasellar masses. Periodic alternating nystagmus is a remarkable horizontal jerking that periodically (every 90 seconds or so) changes direction, interposed with a brief neutral period during which the eyes show no nystagmus or jerk downward. Alternating nystagmus is seen with lesions in the lower brainstem but has also been reported with Creutzfeldt-Jakob disease, hepatic encephalopathy, lesions of the cerebellar nodulus, carcinomatous meningitis, and a large number of other processes. It differs from ping-pong gaze, which is a saccadic variant with a more rapid alternating of gaze from side to side and usually the result of bilateral cerebral strokes. So-called palatal nystagmus, which is really a tremor, is due to a lesion of the central tegmental tract and may be accompanied by a convergence-retraction nystagmus that has the same beat as the palatal and pharyngeal muscles, as discussed on page 85. Other Spontaneous Ocular Movements Roving conjugate eye movements are characteristic of light coma. Slow horizontal ocular deviations that shift every few seconds from side to side ("ping-pong gaze") is a form of roving eye movement that occurs with bihemispheric infarctions or sometimes with posterior fossa lesions. Fisher has noted a similar slow, side- toside pendular oscillation of the eyes ("windshield-wiper eyes"). This phenomenon has been associated with bilateral hemispheric lesions that have presumably released a brainstem pacemaker. Ocular bobbing is a term coined by Fisher to describe a distinctive spontaneous fast downward jerk of the eyes followed by a slow upward drift to the midposition. It is observed in comatose patients in whom horizontal eye movements are absent and has been associated most often with large destructive lesions of the pons, less often of the cerebellum. The eye movements may be disconjugate in the vertical plane, especially if there is an associated third nerve palsy on one side. Other spontaneous vertical eye movements have been given a variety of confusing names: atypical bobbing, inverse bobbing, reverse bobbing, and ocular dipping. For the most part, they are observed in coma of metabolic or anoxic origin and in the context of preserved horizontal eye movements (in distinction to ocular bobbing). Ocular dipping is a term we have used to describe an arrhythmic slow conjugate downward movement followed in several seconds by a more rapid upward movement; it occurs spontaneously but may at times be elicited by moving the limbs or neck. Anoxic encephalopathy has been the most common cause, but a few cases have been attributed to drug overdose (Ropper 1981). Oculogyric crisis, formerly associated with postencephalitic parkinsonism, is now most often due to phenothiazine drugs, as discussed earlier. Opsoclonus is the term applied to rapid, conjugate oscillations of the eyes in horizontal, rotatory, and vertical directions, made worse by voluntary movement or the need to fixate the eyes. These movements are continuous and chaotic, without an intersaccadic pause (called by some by the colorful term saccadomania), and are almost unique among disorders of ocular movement in that they persist in sleep. Opsoclonus may also be observed in patients who are intoxicated with antidepressants, anticonvulsants, organophosphates, cocaine, lithium, thallium, and haloperidol; in the nonketotic hyperosmolar state; and in cerebral Whipple disease, where it is coupled with rhythmic jaw movements (oculomasticatory myorhythmia, page 603). Similar movements have been produced in monkeys by creating bilateral lesions in the pretectum. Ocular dysmetria, the analogue of limb dysmetria, consists of an overshoot of the eyes on attempted fixation followed by several cycles of oscillation of diminishing amplitude until fixation is attained. The overshoot may occur on eccentric fixation or on refixation to the primary position of gaze. It probably reflects dysfunction of the anterosuperior vermis and underlying deep cerebellar nuclei. Ocular flutter refers to occasional bursts of very rapid horizontal oscillations around the point of fixation; this abnormality is also associated with cerebellar disease. Flutter at the end of a saccade, called flutter dysmetria (fish-tail nystagmus) has the appearance of dysmetria, but careful analysis indicates that it is probably a different phenomenon. Whereas the inaccurate saccades of ataxia are separated by normal brief pause (intersaccadic interval), flutter dysmetria consists of consecutive saccades without an intersaccadic interval (Zee and Robinson). Opsoclonus, ocular dysmetria, and flutter-like oscillations may occur together, or a patient may show only one or two of these ocular tremors, either simultaneously or in sequence. One hypothesis relates opsoclonus and ocular flutter to a disorder of the saccadic "pause neurons" (see above), but their exact anatomic basis has not been elucidated. Disorders of the Eyelids and Blinking A consideration of oculomotor disorders would be incomplete without reference to the eyelids and blinking. The function of the eyelids is to protect the delicate corneal surfaces against injury and the retinae against glare; this is done by blinking and lacrimation. Eyelid movement is normally coordinated with ocular movement- the upper lids elevate when looking up and descend when looking down. Turning the eyes quickly to the side is usually attended by a single blink, which is necessarily brief so as not to interfere with vision. When the blink duration is prolonged in this context, it is indicative of an abnormally intense effort required to initiate the saccade; usually this is due to frontal lobe or basal ganglionic disease. Closure and opening of the eyelids is accomplished through the reciprocal action of the levator palpebrae and orbicularis oculi muscles. Relaxation of the levator and contraction of the orbicularis effect closure; the reverse action of these muscles effects opening of the closed eyelids. The levator is innervated by the oculomotor nerve, and the orbicularis by the facial nerve. The trigeminal nerves provide sensation to the eyelids and are also the afferent limbs of corneal and palpebral reflexes. Central mechanisms for the control of blinking, in addition to the reflexive brainstem connections between the third, fifth, and seventh nerve nuclei, include the cerebrum, basal ganglia, and hypothalamus. The eyelids are kept open by the tonic contraction of the levator muscles, which overcomes the elastic properties of the periorbital muscles. The eyelids close during sleep and certain altered states of consciousness due to relaxation of the levator muscles. Blinking occurs irregularly at a rate of 12 to 20 times a minute, the frequency varying with the state of concentration and with emotion. The natural stimuli for the blink reflex (blinking is always bilateral) are corneal contact (corneal reflex), a tap on the brow or around the eye, visual threat, an unexpected loud sound, and, as indicated above, turning of the eyes to one side. There is normally a rapid adaptation of blink to visual and auditory stimuli but not to corneal stimulation. Electromyography of the orbicularis oculi reveals two components of the blink response, an early and late one, a feature that is readily corroborated by clinical observation. The early response consists of only a slight movement of the upper lids; the immediately following response is more forceful and approximates the upper and lower lids. Whereas the early part of the blink reflex is beyond volitional control, the second part can be inhibited voluntarily. Blepharospasm, an excessive and forceful closure of the lids, which is described on page 93, is a common disorder that occurs in isolation or as part of a number of dyskinesias and druginduced movement disorders. Increased blink frequency occurs with corneal irritation, with sensitization of trigeminal nerve endings, and in oculofacial dyskinetic syndromes, such as blepharospasm. A reduced frequency of blinking (10 per minute) is characteristic of progressive supranuclear palsy and Parkinson disease. In these cases, adaptation to repeated supraorbital tapping at a rate of about 1 per second is impaired; therefore the patient continues to blink with each tap on the forehead or glabella. The failure to inhibit this response is referred to as the glabellar or Myerson sign. A lesion of the oculomotor nerve, by paralyzing the levator muscle, causes ptosis, i. Aberrant regeneration of the third nerve after an injury may result in a condition wherein the upper lid retracts on lateral or downward gaze (pseudo von Graefe sign). The Gunn "jaw-winking" phenomenon is a synkinesis that may also occur after aberrant regeneration of the facial nerve but is otherwise a congenital and sometimes hereditary anomaly in which a ptotic eyelid retracts momentarily when the mouth is opened or the jaw is moved to one side. In other cases, inhibition of the levator muscle and ptosis occurs with opening of the mouth ("inverse Marcus Gunn phenomenon," or Marin Amat syndrome). A useful clinical rule is that a combined paralysis of the levator and orbicularis oculi muscles. This is because the third and seventh cranial nerves are rarely affected together in peripheral nerve or brainstem disease. An infrequent but overlooked cause of unilateral ptosis is a dehiscence of the tarsal muscle attachment; it can be identified by the loss of the upper lid fold just below the brow. Bilateral ptosis is a characteristic feature of certain muscular dystrophies and myasthenia gravis; congenital ptosis and progressive sagging of the upper lids in the elderly are other common forms.
Do NOT go into rough or turbulent water that may endanger you.
Age and general health
Nutritional deficiencies, especially niacin, thiamine, vitamin C, or vitamin B12
Disfigurement
Very low levels ofvitamin D
Fatigue
Did you recently hurt your eye?
Clicking
Changes in menstrual bleeding
Decompression of the nerve where it enters the spinoglenoid notch relieves the condition treatment 911 generic betahistine 16 mg without prescription. Axillary Nerve this nerve arises from the posterior cord of the brachial plexus (mainly from the C5 root medications prolonged qt generic betahistine 16 mg with visa, with a smaller contribution from C6) and supplies the teres minor and deltoid muscles medications used to treat bipolar discount 16 mg betahistine fast delivery. It may be involved in dislocations of the shoulder joint medications ok to take while breastfeeding cheap betahistine 16mg overnight delivery, fractures of the neck of the humerus treatment 8th march buy betahistine 16mg with mastercard, serum- and vaccine-induced neuropathies medications like prozac generic betahistine 16mg with mastercard, and brachial neuritis; in other instances treatment ear infection buy 16 mg betahistine amex, no cause may be apparent symptoms when pregnant purchase 16mg betahistine visa. Musculocutaneous Nerve the origin of this nerve is from the fifth and sixth cervical roots. It is a branch of the lateral cord of the brachial plexus and innervates the biceps brachii, brachialis, and coracobrachialis muscles. Lesions of the nerve result in wasting of these muscles and weakness of flexion of the supinated forearm. Sensation may be impaired along the radial and volar aspects of the forearm (lateral cutaneous nerve). Radial Nerve this nerve is derived from the sixth to eighth (mainly the seventh) cervical roots and is the distal extension of the posterior cord of the brachial plexus. It innervates the triceps, brachioradialis, and supinator muscles and continues below the elbow as the posterior interosseous nerve, which innervates the extensor muscles of the wrist and fingers, the abductor of the thumb, and the extensors of the fingers at both joints. A complete proximal radial nerve lesion results in paralysis of extension of the elbow, flexion of the elbow with the forearm midway between pronation and supination (due to paralysis of the brachioradialis muscle), supination of the forearm, extension of the wrist and fingers, and extension and abduction of the thumb in the plane of the palm. If the lesion is confined to the posterior interosseous nerve, only the extensors of the wrist and fingers are affected. Sensation is impaired over the posterior aspects of the forearm and over a small area on the radial aspect of the dorsum of the hand. The radial nerve may be compressed in the axilla ("crutch" palsy) but more frequently at a lower point, where the nerve winds around the humerus (see Table 46-8); pressure palsies incurred during an alcoholic stupor and fractures of the humerus commonly injure the nerve at the site of injury. It is susceptible to lead intoxication and is frequently involved as part of a neuralgic amyotrophy. Median Nerve this nerve originates from the fifth cervical to the first thoracic roots but mainly from the sixth cervical root and is formed by the union of the medial and lateral cords of the brachial plexus. It innervates the pronators of the forearm, long finger flexors, and abductor and opponens muscles of the thumb and is a sensory nerve to the palmar aspect of the hand. Complete interruption of the median nerve results in inability to pronate the forearm or flex the hand in a radial direction, paralysis of flexion of the index finger and terminal phalanx of the thumb, weakness of flexion of the remaining fingers, weakness of opposition and abduction of the thumb in the plane at a right angle to the palm (abductor and flexor pollicis brevis), and sensory impairment over the radial two-thirds of the palm and dorsum of the distal phalanges of the index and third fingers. The nerve may be injured in the axilla by dislocation of the shoulder and in any part of its course by stab, gunshot, or other types of wounds. Incomplete lesions of the median nerve between the axilla and wrist may result in causalgia (see further on). Carpal Tunnel Syndrome Compression of the median nerve at the wrist (carpal tunnel syndrome) is the most common disorder affecting the median nerve and the most frequent nerve entrapment syndrome. This is usually due to excessive use of the hands and occupational exposure to repeated trauma. In elderly individuals, the cause of the carpal tunnel syndrome is often not apparent. According to Kremer and colleagues, it was McArdle, in 1949, who first suggested that the cause of this syndrome was a compression of the median nerve at the wrist and that the symptoms would be relieved by division of the flexor retinaculum forming the ventral wall of the carpal tunnel. Dysesthesias and pain in the fingers, referred to for many years as "acroparesthesiae" and attributed to cervical ribs, came to be recognized as a syndrome of median nerve compression only in the early 1950s. The syndrome is essentially a sensory one; the loss or impairment of superficial sensation affects the palmar aspect of the thumb, and the index, and middle fingers (especially the index finger) and may or may not split the ring finger (splitting does not occur with a plexus or root lesion). Weakness and atrophy of the abductor pollicis brevis and other medianinnervated muscles occur in only the most advanced cases of compression. Electrophysiologic testing confirms the diagnosis by demonstrating prolonged sensory conduction across the wrist and explains cases in which operation has failed (see also the review by Stevens). The Phalen maneuver consists of hyperflexion of the wrist for 30 to 60 s- usually performed by opposing the outer surfaces of the hands with the wrists flexed. The Tinel sign is elicited by lightly tapping the volar aspect of the wrist at the transverse carpal ligament (distal to the first wrist crease). Both of these tests are meant to elicit pain or paresthesias over the digits innervated by the median nerve. The sensitivity of these tests is close to 50 percent but their specificity is considerably higher. Other tests involving prolonged pressure over the median nerve have been devised but they are of uncertain value. Treatment Surgical division of the carpal ligament with decompression of the nerve is curative but is required only in severe and protracted cases. Splinting of the wrist, to avoid flexion, almost always relieves the discomfort but denies the patient the full use of the hand for some time. It is a useful temporizing measure, however, as is the injection of hydrocortisone into the carpal tunnel. Treatment of an underlying condition such as arthritis, hypothyroidism, possibly diabetes, is often helpful. Some patients have benefited, paradoxically, from the stopping of corticosteroids or estrogen. Also, some practitioners favor the use of nonsteroid anti-inflammatory medication but we have been generally unimpressed with the results. Most often, splinting and local steroid injections are very satisfactory in the short-term, especially if the symptoms are of recent onset. Another less common site of compression of the median nerve is at the elbow, where the nerve passes between the two heads of the pronator teres, or just above that point behind the bicipital aponeurosis. It gives rise to the pronator syndrome, in which forceful pronation of the forearm produces an aching pain (see Table 468). There is weakness of the abductor pollicis brevis and opponens muscles and numbness of the first three digits and palm. Ulnar Nerve this nerve is derived from the eighth cervical and first thoracic roots. It innervates the ulnar flexor of the wrist, the ulnar half of the deep finger flexors, the adductors and abductors of the fingers, the adductor of the thumb, the third and fourth lumbricals, and muscles of the hypothenar eminence. Complete ulnar paralysis is manifest by a characteristic clawhand deformity; wasting of the small hand muscles results in hyperextension of the fingers at the metacarpophalangeal joints and flexion at the interphalangeal joints. The flexion deformity is most pronounced in the fourth and fifth fingers, since the lumbrical muscles of the second and third fingers, supplied by the median nerve, counteract the deformity. Sensory loss occurs over the fifth finger, the ulnar aspect of the fourth finger, and the ulnar border of the palm. The ulnar nerve is vulnerable to pressure in the axilla from the use of crutches, but it is most commonly injured at the elbow by fracture or dislocation involving the joint. Delayed ("tardive") ulnar palsy may occur many months or years after an injury to the elbow that had resulted in a cubitus valgus deformity of the joint. Because of the deformity, the nerve is stretched in its groove over the ulnar condyle, and its superficial location renders it vulnerable to compression. A shallow ulnar groove, quite apart from abnormalities of the elbow joint, may expose the nerve to compressive injury. Anterior transposition of the ulnar nerve is a simple and effective form of treatment for these types of ulnar palsy. Compression of the nerve may occur just distal to the medial epicondyle, where it runs beneath the aponeurosis of the flexor carpi ulnaris (cubital tunnel). Flexion at the elbow causes a narrowing of the tunnel and constriction of the nerve. This type of ulnar palsy is treated by incising the aponeurotic arch between the olecranon and medial epicondyle. Prolonged pressure on the ulnar part of the palm may result in damage to the deep palmar branch of the ulnar nerve, causing weakness of small hand muscles but no sensory loss. This site is most often implicated in patients who hold tools or implements tightly in the hand for long periods (we have seen it in machinists and professional cake decorators). A characteristic syndrome of burning pain and associated symptoms (causalgia) may follow incomplete lesions of the ulnar nerve (or other major nerves of the limbs) and is described further on. Lumbosacral Plexus and Crural Neuropathies the twelfth thoracic, first to fifth lumbar, and first, second, and third sacral spinal nerve roots compose the lumbosacral plexuses and innervate the muscles of the lower extremities. Lumbosacral Plexus Lesions Extending as it does from the upper lumbar area to the lower sacrum and passing near several lower abdominal and pelvic organs, this plexus is subject to a number of special injuries and diseases, most of them secondary. The cause of involvement may be difficult to ascertain because the primary disease is often not within reach of the palpating fingers, either from the abdominal side or through the anus and vagina; even refined radiologic techniques may not reveal it. The clinical findings help to focus studies on the appropriate part of the lumbosacral plexus. The main effects of upper lumbar plexus lesions are weakness of flexion and adduction of the thigh and extension of the leg, with sensory loss over the anterior thigh and leg; these effects must be distinguished from the symptoms and signs of femoral neuropathy (see later). Lower plexus lesions weaken the posterior thigh, leg, and foot muscles and abolish sensation over the first and second sacral segments (sometimes the lower sacral segments also). Lesions of the entire plexus, which occur infrequently, cause a weakness or paralysis of all leg muscles, with atrophy, areflexia, anesthesia from the toes to the perianal region and autonomic loss with warm, dry skin. The types of lesions that involve the lumbosacral plexus are rather different from those affecting the brachial plexus. Trauma is a rarity except with massive pelvic, spinal, and abdominal injuries because the plexus is so well protected. Occasionally a pelvic fracture will damage the sciatic nerve as it issues from the plexus. In contrast, some part of the plexus may be damaged during surgical procedures on abdominal and pelvic organs, often for reasons that may not be entirely clear. For example, hysterectomy has on a number of occasions led to neurologic consultation in our hospitals because of numbness and weakness of the anterior thigh. Either the cords of the upper part of the plexus or the femoral nerve was compressed by retraction against the psoas muscle or, in vaginal hysterectomy (when thighs are flexed, abducted, and externally rotated), the femoral nerve was compressed against the inguinal ligament. Lumbar sympathectomy has also been associated with upper plexus lesions, of which the most disabling sequelae are burning pain and hypersensitivity of the anterior thigh. Appendectomy, pelvic explorations, and hernial repair may injure branches of the upper plexus (ilioinguinal, iliohypogastric, and genitofemoral nerves), with severe pain and slight sensory loss in the distribution of one of these nerves. Usually there is pain that radiates to the hip, the anterior thigh, and occasionally the flank. Slight weakness in hip flexion and altered sensation over the anterior thigh are found on examination. Plexus involvement with tumors is commonplace and at times presents special difficulties in diagnosis. Carcinoma of either the cervix or prostate may seed itself along the perineurial lymphatics and cause pain in the groin, thigh, knee, or back without much in the way of sensory, motor, or reflex loss. Testicular, uterine, ovarian, and colonic tumors or retroperitoneal lymphomas, by extending along the paravertebral gutter, implicate various parts of the lumbosacral plexus. The neurologic symptoms are projected at a distance in the leg and may or may not be confined to the territory of any one nerve. If all these examinations are negative, exploratory laparotomy may have to be undertaken. In cancer patients, it is sometimes difficult to distinguish the effects of radiation on the lumbosacral plexus from those of metastatic tumor, as is the case in relation to the brachial plexus. Again, the earliest symptom in metastatic lumbosacral plexopathy is usually pain, whereas in radiation plexopathy it is weakness (Thomas et al); the same as pertains in the brachial plexus. Fasciculations and myokymia are more likely to be seen in patients with radiation plexopathy, which seemingly occurs more frequently in patients with diabetic neuropathy. Reference has already been made to femoral nerve injury during parturition, but other puerperal complications are also observed. Back pain in the latter part of pregnancy is common, but there are rare instances in which the patient complains of severe pain in the back of one or both thighs during labor and after delivery has numbness and weakness of the leg muscles, with diminished ankle jerks. Parturitional lumbosacral plexus injuries occur with a frequency of 1 per 2000 deliveries. This type of plexus injury is usually unilateral and is manifest by pain in the thigh and leg and symptoms and signs of involvement of the superior gluteal and sciatic nerves (Feasby et al). The attribution of these symptoms to pressure of the fetal head on the sacral plexus(es) is conjectural. A limited plexopathy, occurring after difficult vaginal delivery, mainly impairs sensation in the perineum and sphincteric function (Ismael et al). Idiopathic Lumbosacral Plexitis In addition to a diabetic type, an idiopathic neuralgic amyotrophy or lumbosacral plexitis, analogous to the brachial variety, is observed from time to time. After causing widespread unilateral or bilateral sensory, motor, and reflex changes in a leg, lumbosacral plexitis may leave the patient with dysesthesias as troublesome as those that follow herpes zoster (which may also occur at this level). Some patients have had an exploration of the cauda equina (for ruptured disc), even though loss of sweating and warmth of the feet should have indicated interruption of autonomic fibers by lesions in peripheral nerves. Diabetic amyotrophy, due to involvement of the lumbar plexus, has a vascular origin, probably inflammatory as discussed in an earlier section (page 1135), and there are also nondiabetic vascular lesions that give rise to identical lumbar and upper leg pain and weakness in proximal muscles. The plexus lesions of polyarteritis nodosa, unilateral or bilateral, may also be manifest as a mononeuropathy multiplex. Mononeuropathy multiplex in diabetic patients is more frequent in our experience when there is an associated occlusive vascular disease of the lower extremities. Diabetic mononeuropathy multiplex is discussed in an earlier part of this chapter and protruded intervertebral disc syndromes are described in Chap. Lateral Cutaneous Nerve of the Thigh this is a sensory nerve that originates from the second and third lumbar roots and supplies the anterolateral aspect of the thigh, from the level of the inguinal ligament almost to the knee. The nerve penetrates the psoas muscle, crosses the iliacus, and passes into the thigh by coursing between the attachments of the lateral part of the inguinal ligament to just anterior to the anterior superior iliac spine. Compression (entrapment) may occur at the point where it passes between the two prongs of attachment of the inguinal ligament. Compression of the nerve results in uncomfortable paresthesias and sensory impairment in its cutaneous distribution, a common condition known as meralgia paresthetica (meros, "thigh"). Usually numbness and mild sensitivity of the skin are the only symptoms, but occasionally there is a persistent distressing burning pain. Perception of touch and pinprick are reduced in the territory of the nerve; there is no weakness of the quadriceps or diminution of the knee jerk. The symptoms are characteristically worsened in certain positions and after prolonged standing or walking. Most often the neuropathy is unilateral; Ecker and Woltman found only 20 percent of their cases to be bilateral. Most of our patients with meralgia paresthetica request no treatment once they learn of its benign character. Weight loss and adjustment of restrictive clothing or correction of habitual postures that might compress the nerve are sometimes helpful. A few with the most painful symptoms have demanded a neurectomy or section of the nerve, but it is always wise to perform a lidocaine block first, so that the patient can decide whether the persistent numbness is preferable. In one specimen of nerve obtained at operation, we found a discrete traumatic neuroma. Hydrocortisone injections at the point of entrapment may have helped in a few cases. Obturator Nerve this nerve arises from the third and fourth and to a lesser extent the second lumbar roots. It supplies the adductors of the thigh and contributes to the innervation of the internal and external rotators. The nerve may be injured by the fetal head or forceps during the course of a difficult labor or compressed by an obturator hernia. Rarely, it is affected with diabetes, polyarteritis nodosa, and osteitis pubis and by retroperitoneal spread of carcinoma of the cervix, uterus, and other tumors (Rogers et al). Femoral Nerve this nerve is formed from the second, third, and fourth lumbar roots. The former supplies the pectineus and sartorius muscles and carries sensation from the anteromedial surface of the thigh; the posterior division provides the motor innervation to the quadriceps and the cutaneous innervation to the medial side of the leg from the knee to the internal malleolus. Following injury to the femoral nerve, there is weakness of extension of the lower leg, wasting of the quadriceps muscle, and failure of fixation of the knee. If the nerve is injured proximal to the origin of the branches to the iliacus and psoas muscles, there is weakness of hip flexion. The adductor of the thigh (innervated by the obturator nerve) is spared, distinguishing femoral neuropathy from an L3 radiculopathy. Usually this is the result of improper placement of retractors, which may compress the nerve directly or indirectly by undue pressure on the psoas muscle. Bleeding into the iliacus muscle or the retroperitoneum, observed in patients receiving anticoagulants and in hemophilia patients, is a relatively common cause of isolated femoral neuropathy (Goodfellow et al). The presenting symptom of iliacus hematoma is pain in the groin spreading to the lumbar region or thigh, in response to which the patient assumes a characteristic posture of flexion and lateral rotation of the hip. A palpable mass in the iliac fossa and the signs of femoral nerve compression (quadriceps weakness and loss of knee jerk) follow in a day or two. Sciatic Nerve this nerve is derived from the fourth and fifth lumbar and first and second sacral roots, for which reason a ruptured disc at any of these levels may simulate sciatic neuropathy (sciatica). The sciatic nerve supplies motor innervation to the hamstring muscles and all the muscles below the knee through its two divisions, the tibial and peroneal nerves (see later); the sciatic nerve conveys sensory impulses from the posterior aspect of the thigh, the posterior and lateral aspects of the leg, and the entire sole. In complete sciatic paralysis, the knee cannot be flexed and all muscles below the knee are paralyzed. Weakness of gluteal muscles and pain in the buttock and posterior thigh point to nerve involvement in the pelvis. Lesions beyond the sciatic notch spare the gluteal muscles but not the hamstrings. Partial compressive lesions are more common and tend to involve peroneal-innervated muscles more than tibial ones, giving the impression of a peroneal palsy. As mentioned, rupture of one of the lower lumbar intervertebral discs is perhaps the most common cause of sciatica, although it does not directly involve the sciatic nerve.
