Q. Hector. Cypress College.
Neu- ing in patients with mild Alzheimer disease: A randomized con- ropathology and apolipoprotein E profle of aged chimpanzees: trolled trial discount 120 mg sildalis with visa. A beta40 is a major profle in streptozotocin rat model for sporadic Alzheimer’s dis- form of beta-amyloid in nonhuman primates buy sildalis 120 mg low price. Hydroxyl radicals discount sildalis online master card, iron best purchase sildalis, oxidative stress, beta) deposition in the brains of aged orangutans. Practical considerations of ge- associated with a reduced risk of Alzheimer disease regardless netic rodent models for neurodegenerative diseases. Pharmacologi- cosaminoglycan mimetics: A therapeutic approach to cerebral cal modulation of Alzheimer’s beta-amyloid precursor protein amyloid angiopathy. Spatial learning and lular damage in rabbits fed with long-term cholesterol-enriched memory as a function of age in the dog. Alzheimer’s disease: discrimination learning ability and beta-amyloid accumulation Initial report of the purifcation and characterization of a novel in the dog. Acetylcho- cological comparison of muscarinic ligands: Historical ver- linesterase accelerates assembly of amyloid-beta-peptides into sus more recent muscarinic M1-preferring receptor agonists. Alzheimer’s fbrils: Possible role of the peripheral site of the Eur J Pharmacol 605, 53-56. Nat Neurosci 7, emergence and progression of a tauopathy in transgenic mice 954-960. Visualization of and clinical function in mild to moderate Alzheimer’s disease A beta 42(43) and A beta 40 in senile plaques with end-specifc patients: Results of a six-month, double-blind, placebo control- A beta monoclonals: Evidence that an initially deposited spe- led, dose ranging study. Treatment servation of the sequence of the Alzheimer’s disease amyloid with the selective muscarinic m1 agonist talsaclidine decreases peptide in dog, polar bear and fve other mammals by cross-spe- cerebrospinal fuid levels of A beta 42 in patients with Alzhe- cies polymerase chain reaction analysis. Plaque- effects of galantamine on cognitive function in Alzheimer’s independent disruption of neural circuits in Alzheimer’s disease disease: A large-scale international retrospective study. Correlative mem- 110417 ory defcits, Abeta elevation, and amyloid plaques in transgenic Kiatipattanasakul, W. Identifying and validating biomarkers for in the brain of an aged albino cynomolgus monkey (Macaca Alzheimer’s disease. Direct reprogramming into desired cell types by participation in cardiovascular randomized controlled trials defned factors. Chronic admin- lary tangles, amyotrophy and progressive motor disturbance istration of R-furbiprofen attenuates learning impairments in in mice expressing mutant (P301L) tau protein. Compara- neuroprotective actions of (-)- and (+)-phenserine, candidate tive analysis of amyloid-beta chemical structure and amyloid drugs for Alzheimer’s disease. M007859200 ent neuroplasticity mechanisms in Alzheimer Tg2576 mice fol- Landsberg, G. Therapeutic agents for the treatment of lowing modulation of brain amyloid-beta levels. Caloric in- basis of C-terminal beta-amyloid peptide binding by the anti- take and the risk of Alzheimer disease. Arch Neurol 60, sociated with reduced risk for incident dementia among persons 203-208. Rejuvenation Res pathology and glial responses to neuronal injury precede the 11, 321-332. Meman- thology in transgenic mice overexpressing V717F beta-amyloid tine improves spatial learning in a transgenic mouse model precursor protein. Infam- cognitive function in amyloid precursor protein-transgenic and matory responses to amyloidosis in a transgenic mouse model nontransgenic mice. Perturbed notypic changes in transgenic mice that overexpress different endoplasmic reticulum function, synaptic apoptosis and the mutants of amyloid precursor protein in brain. Metrifonate effects 5260%2812%2900367-6/fulltext on acetylcholine and biogenic amines in rat cortex. J Med Chem 51, 7348- tion of fsh and n-3 fatty acids and risk of incident Alzheimer 7351. R800030200 both mutant amyloid precursor protein and mutant presenilin 1 Mucke, L. Consensus recommendations for the postmortem di- in cognition and mortality in relation to exercise in late life: agnosis of Alzheimer’s disease. Has inhibition in Alzheimer’s disease destroying a splice acceptor site in the of Abeta production adequately been tested as therapeutic ap- presenilin-1 gene. Physical activ- in transgenic mice with fve familial Alzheimer’s disease mu- ity and cognitive trajectories in cognitively normal adults: The tations: Potential factors in amyloid plaque formation. Triple-trans- of gamma-secretase inhibition on the amyloid beta isoform pat- genic model of Alzheimer’s disease with plaques and tangles: tern in a mouse model of Alzheimer’s disease. Proteomic identifca- formance and biochemical markers in septum, hippocampus tion of brain proteins in the canine model of human aging fol- and striatum of rats after an i. Care arrangements presenilin 2 transgenic mouse: Effect on an age-dependent in- for people with dementia in developing countries. Amyloid- and amyotrophy in mice transgenic for human four-repeat tau based immunotherapy for Alzheimer’s disease in the time of protein. Effcacy and 0087-3 safety of rivastigmine in patients with Alzheimer’s disease: in- Radak, Z. N Engl J Med 348, 1333- 089: Pharmacological properties of a neuronal nicotinic acetyl- 1341. Arachidonic and despite reductions in amyloid-beta levels: Implications for the docosahexaenoic acids are biosynthesized from their 18-carbon treatment of Alzheimer disease. Alzhe- factors for beta-amyloid deposition in healthy aging: Vascular imer-like changes in protein kinase B and glycogen synthase and genetic effects. What tions in a gene on chromosome 1 related to the Alzheimer’s have we learned from the streptozotocin-induced animal model disease type 3 gene. Metal sor protein alpha quantifcation: Preclinical and clinical appli- protein attenuating compounds for the treatment of Alzheimer’s cations in Alzheimer’s disease. Truncated membrane domain that contains decreased levels of glycero- beta-amyloid peptide species in pre-clinical Alzheimer’s dis- phospholipids and sphingomyelin. Production of the of dementia and Alzheimer disease: The Framingham Heart Alzheimer amyloid beta protein by normal proteolytic process- Study. Insights drial dysfunction and tau hyperphosphorylation in Ts1Cje, a into Alzheimer disease pathogenesis from studies in transgenic mouse model for Down syndrome. The effect of aging on pars netic linkage evidence for a familial Alzheimer’s disease locus compacta of the substantia nigra in rhesus monkey. Oxidative stress in neu- with amyloid-beta attenuates Alzheimer-disease-like pathol- rodegenerative diseases. Alzhe- polyphenol-derived protection against neurotoxic beta-amyloid imer’s disease-like tau neuropathology leads to memory defcits protein: From molecular to clinical. J Alzheimers Dis 37, neuron loss exceeds amyloid plaque load in a transgenic mouse 197-215. J Nutr Health Aging 13, 264- dative damage in amyloid beta protein precursor-mediated cell 267. Trace amounts of copper A cross-national study of co-resident spouse carers for people in water induce beta-amyloid plaques and learning defcits in a with Alzheimer’s disease: I-Factors associated with carer bur- rabbit model of Alzheimer’s disease. Age-related tion in the tau gene in familial multiple system tauopathy with progression of tau pathology in brains of baboons. Caregiving as a risk factor inent axonopathy in the brain and spinal cord of transgenic mice for mortality: The Caregiver health effects study. Production of Apolipoprotein E: High-avidity binding to beta-amyloid and in- recombinant human type I procollagen homotrimer in the mam- creased frequency of type 4 allele in late-onset familial Alzhe- mary gland of transgenic mice. Lithium, a common drug thiofavin S-positive amyloid deposits in transgenic mice and for bipolar disorder treatment, regulates amyloid-beta precursor Alzheimer’s disease. Am J Clin Nutr 85, long-acting cholinesterase inhibitor reverses spatial memory 1142-1147. Curr Alz- thamine, an acetylcholinesterase inhibitor: A time course of the heimer Res 8, 34-58. Ann Clin Biochem 46, generation with tau accumulation in a transgenic mouse ex- 235-240. The oligomer- (Canis familiaris) using two versions of a spatial list learning ization of amyloid beta-protein begins intracellularly in cells de- paradigm. Ann Neurol 30, protection of acetylcholinergic basal forebrain neurons by me- 572-580. The relationship between Abeta and memory in the Altex 31, 3/14 301 Cava n a u g h e t a l.
Sudden death can occur from respiratory arrest or irregular heart rhythms that are often difficult to treat even if medical care is quickly available proven sildalis 120mg. The acute signs and symptoms of inhalant abuse resemble a combination of alcohol and marijuana intoxication purchase 120mg sildalis fast delivery. Physical symptoms of withdrawal from inhalants include hallucinations purchase sildalis australia, nausea cheap 120 mg sildalis otc, excessive sweating, hand tremors, muscle cramps, headaches, chills and delirium tremens. Thirty to forty days of detoxification is often required, and relapse is frequent. Treatment During the acute episode, if physically stable but emotionally distraught, the patient can be treated by “talking-down,” recognizing the possibility of hostile outbursts. As with other substance abuse problems, a drug/alcohol assessment screening by a qualified screener as soon as the ship arrives in homeport may be indicated. Substances of abuse have both short- and long- term effects on the health of the individual crew member. Serious medical consequences, including death, can result from unintentional overdoses, especially if more than one drug is taken at a time. An intoxicated crew member can endanger the ship, its mission, and the entire crew. The Captain’s leadership is critical, and the responsible behavior of everyone aboard is essential. Treatment of dental emergencies is challenging under austere conditions and/or in minimally dentally equipped sick bays. However, recent dental treatment, such as tooth extractions, can also contribute to dental emergencies when there are post-operative complications. A differential diagnosis is important to identify or rule out active infection that could be treated, or, if untreated, could become life threatening. Many oral diseases result in infection but prompt diagnosis and treatment can help to avoid serious complications. Also, pain arising from non-dental sources such as myofascial inflammation, temporomandibular dysfunction, sinusitis, neuralgias, and the ears must always be considered in the differential diagnosis. An organized approach to find the cause of the pain will help to make the diagnosis and determine the treatment. The following should be considered: Location: Quadrant – Upper Left, Lower Left, Upper Right, Lower Right Duration: Onset and length of time Type of Pain: Sensitivity to temperature, mastication, sweets, and/or spontaneous pain Swelling: Diffuse vs. It is always wise to consider a radio consult with a dentist or oral surgeon when treating a dental emergency. Additional dental information can be found at the American Dental Association website at: http://www. The interproximal gums (the gums between the teeth) in the lower anterior region are most often affected. Stress to the patient the need for good nutrition, oral hygiene and plenty of rest. Have patient swish with 1 cap full of chlorhexidine (Peridex) for 30 sec and expectorate, b. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. It results if the clot that forms after tooth extraction is lost too early (usually 2-3 days after surgery). The extraction site (socket) will have a grayish appearance and there is usually a bad odor. Treatment: Use sterile water or saline to gently irrigate the socket and remove necrotic debris. Apply a palliative medication: Nu-gauze slightly moistened with Eugenol placed in the socket for 24 hours This should relieve the intense ache within 30 - 40 minutes. Continue to change the dressing every 24 hours for 3 days, gently irrigating the extraction site with sterile saline before replacing dressing. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. Notify dental clinic of any persistent symptoms and arrange for patient to be seen as soon as possible. Treatment: Administer topical anesthetic, lidocaine viscous (oral preparation), 1 tablespoon four times a day (before meals and at bedtime) to provide short-term relief and to facilitate eating if patient has multiple ulcers. Apply a protective dental paste (Orabase) to individual ulcers 4 times a day (after meals and at bedtime) to prevent irritation by the teeth and oral fluids. Treatment: Immediate Action: Examine socket area and gums for any obvious bone fragment or deformity (remove any loose deformity). Place a small amount of wax on the avulsed tooth and adjacent teeth to help stabilize tooth. If Save A Tooth solution is not available, other storage solution options include the following (in order of preference): milk, saline, saliva, or sterile water. If unable to move tooth into original position, place gauze between posterior teeth as a jaw rest. Contact dentist to determine evacuation priority and modality Administer analgesic P. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. Initial caries appears as a white spot on the tooth or a halo-like dark shadow in the enamel. Caries that produce pain are usually in the advanced stages, appearing as very large dark areas or even as a wide-open hole in the tooth. If symptoms are not relieved with analgesics, notify dental clinic and arrange for patient to be seen as soon as possible. The fracture can involve just the enamel or can be so severe as to involve the pulp, where the nerves and blood vessels are located. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. Notify dental clinic and arrange for patient to make a routine scheduled appointment. As the abscess forms, pressure form the swelling and pus formation causes the tooth to be pushed up in its socket. If the built up pus has no where to drain, the jaw may swell and the patient will have much pain. Treatment: Immediate Action: If obvious superficial fluctuant swelling is present, induce drainage with #11 Bard Parker. Acetaminophen with Codeine (Tylenol# 3), 1 - 2 tablets q 4-6 hours for severe pain. Stress to the patient the need for good oral hygiene to improve the condition of the gum in spite of the pain or bleeding. Dispense an irrigation syringe to patient and show them how to irrigate area four times a day with saline solution. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. Treatment: Immediate Action: If possible, remove obvious plaque buildup by irrigation of the area using large amounts of saline and an irrigation syringe. Stress to the patient the need for good oral hygiene to improve the condition of the gum in spite of the pain or bleeding. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. Acetaminophen with codeine (Tylenol # 3), 1 - 2 tablets q 4-6 hours for severe pain. Clinical Note: If symptoms do not improve in 24 hours, notify dental clinic and arrange for patient to make a routine scheduled appointment. Stainless steel plastic filling instrument for application of cements, dressings, etc. Topical anesthetic 20% Benzocaine gel 30gm bottles (2) - used for topical mucosal anesthetic 10.
Cutaneous leishmaniasis prevalence rates vary considerably discount sildalis 120mg amex, but most endemic countries are reporting an increase in cases or an expansion in the disease’s distribution cheap sildalis uk. For example order 120 mg sildalis visa, in 1972 purchase sildalis on line amex, a total of 22,368 human cases of leishmaniasis (cutaneous and visceral) were reported in the Americas, 20,348 of them from Mesoamerica, espe- cially Guatemala (29. Since 1987, Brazil has been reporting between 23,000 and 26,000 cases of cutaneous leishmaniasis annually, with 2,511 cases of visceral leishmaniasis in 1985 alone (Lacerda, 1994). The Disease in Man: Cutaneous leishmaniasis is a polymorphous disease that may affect only the skin or both the skin and the mucous membranes. It manifests initially as itchy erythematous lesions, which later form papules and then painless ulcers. There may be one or many lesions, and they may sometimes be nonulcerative and diffuse. Though the lesions generally heal spontaneously within weeks or months, they may persist for as long as a year, or more. Spontaneous healing of leishmaniasis in man has been shown to depend on cell-mediated immunity and production of gamma interferon (Carvalho et al. In the Americas, the disease occurs in several clinical forms, depending mainly, but not solely, on the species of the eti- ologic agent involved. It causes a benign infection with only one or a few skin ulcers, known as chiclero ulcer, chiclero ear, or bay sore. The lesion is usually located on the earflap or, less often, on the face or extremities. It begins with an ery- thematous papule that then ulcerates and, when the scab comes off, bleeds easily. The lesions on the earflap are deforming, tend to be chronic, and may last many years, while those on other parts of the body heal spontaneously in about six months. A distinctive feature of this form of cutaneous leishmaniasis is that it may spread to the lymph nodes, though this very rarely occurs. In Mexico, no cases of mucocuta- neous leishmaniasis have been detected, but two or three cases of cutaneous lesions that invaded the contiguous mucosa have been reported. The vectors are not espe- cially attracted to man, and the main victims tend to be people who spend a lot of time in the forest, the vector’s habitat, such as the gum tappers (chicleros)who work there during the rainy season when phlebotomine flies are plentiful. Human cases due to this agent are rare because the vec- tors are nocturnal and not normally anthropophilic, and they inhabit marshy areas where man does not ordinarily live. Around 30% of patients have diffuse cutaneous lesions characterized by thickening of the skin in the form of scattered plaques, papules, or nodules, found mainly on the face and legs. This diffuse form of leishmaniasis has been described in Venezuela, but it also occurs in other areas. Patients with diffuse cutaneous leish- maniasis are anergic and do not react to the Montenegro skin test. Healthy volunteers inoculated with parasites from patients with diffuse cutaneous leishmaniasis developed a localized lesion at the inoculation site which healed without sequelae. For that reason, the occurrence of this form is believed to be due more to deficient immune response in the host than to some special property of the parasite. The disease begins with a papular lesion on the face or extrem- ities that may develop into a painless ulcer that seldom heals spontaneously. A char- acteristic feature of this form is metastasis to the mucocutaneous parts of the body. A sizable proportion of untreated patients develop lesions on the nasal septum, mouth, nasopharynx, and, sometimes, even the anorectal region, penis, scrotum, and vulva. These metastases may occur simultaneously with the primary lesion or, more often, much later, and may cause severe destruction of the affected tissue, disfigur- ing the patient. Despite these descriptions, most clinical physicians indicate that it is very diffi- cult to differentiate between subspecies of leishmanias based only on the lesions they cause. The lesion begins as a papule on the exposed parts of the body (face and extremities), which develops into a wet ulcer. The disease lasts two to eight months, and fibrosis during spontaneous healing leaves a permanent scar. The initial papule develops slowly, and ulceration, when it occurs, is also slow to develop. Owing to the diffi- culty of identifying the parasite species, the etiologic agent of leishmaniasis in dogs is sometimes called simply L. Regardless of which species causes the infection, dogs often exhibit both cutaneous and visceral manifestations. In endemic areas, leishmaniasis may also occur in equines, which develop nodular lesions and sometimes scabs or ulcers, but only on or around the earflap. In Venezuela, of 116 donkeys examined, 28 had one or more ulcerous lesions and 17 (15%) had positive microscopy. Based on its behavior in hamsters and culture media, the authors classified the agent as L. Lesions consist of swellings with hair loss and, sometimes, ulcers, in which the pres- ence of amastigotes can be demonstrated. In these cases, the skin remains normal in appearance but the parasites are dispersed in the dermis. The parasites can be cultured from blood, viscera (spleen, liver), and apparently normal skin. Source of Infection and Mode of Transmission: In the Americas, the reservoirs of cutaneous leishmaniasis are generally rodents or edentate animals (Table 1). The infection is transmitted from one wild animal to another by means of phlebotomine flies of the genus Lutzomyia. Humans are infected accidentally by the bite of these phlebotomines when they enter enzootic areas in the jungle. However, Lainson (1983) suspected that dogs are actually a secondary host of this infection (uta) and that the primary host is a wild animal. In some areas of the Americas, the relative roles of the various infected animal species have not been clearly defined. Infected colonies of this desert or semidesert rodent have been found in Iran, the southern part of the former Soviet Union, and from northern Afghanistan to Mongolia. In north- western India and in Israel and Morocco, the reservoirs are Meriones spp. In Algeria, northwestern Libya, and Israel, Psammomys obesus serves as the reservoir, while in Ethiopia and Senegal, the reser- voirs are species of Mastomys, Tatera, and Arvicanthis. Lainson (1982) does not share that opinion, however, pointing out that person-to-person transmission is unlikely, since this agent causes few skin lesions in humans and those lesions con- tain only scant numbers of amastigotes. Humans are accidental hosts who acquire the infection when they enter enzootic forest areas for occupational purposes (e. Cutaneous leishmaniasis may be a serious problem in rural settlements within the jungle. Permanent human settlements in enzootic areas generate significant ecological changes, especially deforestation, replacement of wildlife with domestic animals, and replacement or modification in the prevalence of some insects as species better adapted to the new environment become dominant. These ecological changes also modify the epidemiology of cutaneous leishmaniasis: in Vale do Ribeira, São Paulo, Brazil, 80% of cutaneous leishmaniasis patients worked near their homes and had no contact with the jungle. The devastation of the natural environment altered the species composition of the phlebotomine population in that region and Psychodopygus intermedius—a species that prefers secondary growth, enters human dwellings, and is anthropophilic—became dominant (Tolezano et al. In the western-central region of Venezuela, the disease used to occur exclusively among the inhabitants of villages located near mountainous areas with dense vege- tation. However, cases have been diagnosed in several neighborhoods on the out- skirts of the city of Barquisimeto (Bonfante-Garrido et al. It is not yet known whether this was due to some ecological change, but the appearance of the disease in an urban environment shows that cutaneous leishmaniasis is not always sylvatic or rural and that its epidemiology is changing. Diagnosis: The simplest specific diagnostic method consists of confirming the presence of amastigotes in lesions. For that purpose, the lesion is cleaned with 70% alcohol to remove any necrotic matter. Then, a sample is taken from the edge or base of the lesion (nodule or ulcer of the skin or mucosa) by aspiration, scraping, or biopsy. The sample is mounted on a slide and stained using the Giemsa or Wright technique. Numerous amastigotes may be seen in the case of lesions that are recent or active, but in lesions that are chronic or healing, it can be difficult or impossible to demonstrate the presence of parasites by direct smear microscopy or biopsy. Parasitologic diagnosis is especially difficult in the mucocutaneous form (Cuba Cuba et al.
A good rule of thumb is that if a person’s family would not allow him to pick up children from school then he does not belong on the road purchase sildalis 120 mg visa. Family members may fear the person’s reaction to their opinions and should be given a chance to speak to the physician alone sildalis 120 mg fast delivery. They may need advice and support to help them feel strong enough to take the necessary steps cheap 120mg sildalis visa. Individuals and families should be encouraged to think ahead and develop a plan for driving cessation that addresses questions such as “Is the person living in an accessible area? In life and death matters such as this purchase sildalis master card, the instruction to stop driving is not a recommendation. The physician must be willing to expend considerable emotional goodwill on this issue or even to lose the person from her practice entirely. A recalcitrant individual should be told that the assessment of him as an unsafe driver and the explicit instruction to stop will be entered into his permanent medical record, and that the doctor will not support him if an accident occurs. In especially problematic cases it may be necessary to have the person’s license suspended over his objections, or even to have the car impounded. The doctor’s responsibility regarding unsafe drivers will vary by state, province or country. In some municipalities, physicians are obligated to report individuals who are unsafe to drive because of certain medical conditions or unsafe drivers in general. In other areas, to do so would constitute a breach of doctor/patient confdentiality. Confdentiality is not an absolute right, and it is sometimes trumped by a physician’s duty to the life and safety of the individual and the safety of the public. When there is no other alternative, it may be necessary for a physician to deliberately breach confdentiality to report a person’s behavior to the authorities. The most recognized motor symptom is chorea, but a number of additional movement disorders occur, including dystonia, bradykinesia, rigidity, myoclonus, tics, and tremor. Additional late stage challenges include bowel and bladder incontinence, moderate to severe weight loss, and pain. While disease modifying therapies are not yet available, a number of effective treatments exist for symptomatic management. Chorea is characterized by involuntary movements which are often sudden, irregular and purposeless or semi-purposeful. The movements are often more prominent in the extremities early in the disease, but may eventually include facial grimacing, eyelid elevation, neck, shoulder, trunk, and leg movements as the disease progresses. Chorea typically increases in frequency and amplitude over time, and may peak about 10 years after disease onset. Because involuntary movements may cease at the start of the physical examination, the physician should take note of their presence while obtaining the history. The total chorea score is the sum of the scores for each body region, and can range from 0 – 28. Unifed Huntington’s Disease Rating Scale Motor Assessment Chorea Scale Body Region Severity Face 0 Absent Bucco-oral-lingual 1 Slight/intermittent Trunk 2 Mild/common or moderate/intermittent Right upper extremity 3 Moderate/common Left upper extremity 4 Marked/prolonged Right lower extremity Total score: Sum of scores for each body region Range = 0 - 28 Left lower extremity Symptoms of chorea can range from absent to severe. Chorea in the legs may result in a lurching gait, sometimes with brief fexion of the knees. Individuals who have mild chorea that primarily limits sleep may beneft from low-dose long-acting benzodiazepines such as diazepam or clonazepam at bedtime. Facial and bucco-oro-lingual chorea can lead to repeated tongue and lip injuries, impairing nutritional status and hydration. Individuals with severe chorea develop a downward spiral with pain, tissue injury, weight loss, diffculty concentrating and communicating, and growing dependence on caregivers. Adaptive chairs, toilet seats, low beds, and padding of the environment can be helpful in the home or in the long-term care facility. An occupational therapist can help the family identify suppliers of equipment, and to consider other safety issues within and outside the home. Strategies to reduce chorea include stress reduction and management of mood disorders. Having the caregiver set up routines and schedules that allow extra time for dressing, hygiene, meals and daily activities can be helpful. Symptoms that indicate the need for possible pharmacologic management of chorea include muscle pain, frequent dropping of items, repetitive injuries, falls associated with chorea of the trunk and limbs, poor sleep, and weight loss. Individuals with a total chorea score of 10 or greater may be candidates for pharmacologic treatment. Thetrabenazine is a highly effective treatment, reducing the total chorea score by 5 points in a double-blind, placebo controlled trial. The mechanism of action is depletion of dopamine release by presynaptic striatal neurons. Side effects include sedation, depression, akathisia, and worsening of voluntary motor control. About 20% of individuals in the placebo-controlled trial experienced new onset or worsening of depression, and there was one completed suicide. Physicians must discuss this risk with individuals and their caregivers, and clinical monitoring must be provided. Physicians are also cautioned about the potential risk of tardive dyskinesia or neuroleptic malignant syndrome, although neither occurred in the 12-week randomized trial. The principle of “starting low and going slow” with dose titration helps determine the lowest effective dose and reduces unwanted side effects. In the double-blind study, doses of 50 mg/day were as effective as higher doses, but in people with severe chorea, higher doses may be necessary. Individuals who do not tolerate tetrabenazine, or have other contraindications to its use, may beneft from off-label use of neuroleptics for reduction in chorea. Some atypical neuroleptics such as olanzapine and risperidone may also be effective. The atypical neuroleptics, quetiapine and clozapine, do not block dopamine D2 receptors and are generally ineffective for chorea. Side effects of neuroleptics include apathy, sedation, akathisia, worsening of voluntary motor control, tardive dyskinesia and neuroleptic malignant syndrome. Additional side effects of atypical neuroleptics include weight gain and metabolic syndrome. Some individuals will require increasing doses of anti-chorea medications over time. Dystonia Dystonia is characterized by a repetitive, abnormal pattern of muscle contraction frequently associated with a twisting quality. Trunk dystonia may, at times, be an early symptom and can cause signifcant back pain. Careful monitoring for hallucinations and psychosis is necessary when using dopaminergic agents. Loss of facial expressivity, absence of arm swing, diffculty with fnger tapping and rapid alternating movements and gait slowness are quite common, and worsen with disease progression. Bradykinesia may coexist with, but be diffcult to recognize in the presence of additional hyperkinetic fndings of chorea and dystonia. As noted above, careful monitoring for hallucinations and psychosis is recommended when these agents are used. Tremor is a rhythmic oscillating movement present at rest, with posture, or with voluntary movements. Neuroleptic drug dose reduction or change to an atypical agent should be considered. Rigidity may be improved by reduction or cessation of tetrabenazine or neuroleptic drugs, or by benzodiazepines, baclofen and possibly by dopaminergic drugs. This symptom starts early in the disease, progresses inexorably, and correlates with disability. Slow initiation and velocity of saccadic eye movements are early signs of voluntary movement impairment. Initial exam fndings may include slowness in fnger tapping and rapid alternating movements of the hands. As the disease progresses, fnger tapping becomes more irregular and arrests in movement appear. They are often mute, akinetic, rigid, and dystonic, with hyper refexia and extensor plantar refexes.