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The misalignment may be horizontal or vertical resulting in esotropia (one eye tumor and tumor-like conditions is relatively convergent) compazine 5mg generic medications not to be crushed, exotropia (one eye is relatively divergent; discount 5mg compazine otc symptoms bipolar disorder. In addition 5 mg compazine visa treatment yeast infection men, deviations may be These are painless order 5mg compazine with mastercard symptoms jock itch, cystic masses usually found around the concomitant or incomitant. Concomitant deviations do not orbit at birth, near the medial or lateral part of the eyebrow. They may leak after trauma; extruded sebaceous material produces inflammation and pain. While periorbital der- moids are superficial, and thus simpler to remove surgically, orbital ones require an orbital approach. It has been already discussed in 1022 Chapter 12 on “Malignancies in Children”—(Chapter 12. All such children should be urgently referred to Watering from the eyes an ophthalmologist. The cause of cataract, in about a third of the cases, is congenital dacryocystitis obscure; a quarter show autosomal-dominant inheritance. This is a result of incomplete canalization of the nasolacrimal Bilateral cataracts can be due to infection during pregnancy duct, usually due to epithelial debris, membranes or (rubella, chicken pox, cytomegalovirus, herpes, syphilis and valves in the duct. There is excessive unilateral or bilateral toxoplasmosis), galactosemia, diabetes, hypoglycemia, watering soon after birth. The lacrimal sac may distend with hypocalcemia, drugs (corticosteroids) and trisomy or accumulated secretions to form a palpable, cystic mass myotonic dystrophy. Pressure be associated with ocular abnormalities like posterior over this mass causes mucopus to regurgitate through the lenticonus and persistent hyperplastic primary vitreous. Ocular trauma is an important cause of unilateral cataract the condition is amenable to conservative treatment in older children. Sustained pressure Some types of cataracts are visually insignificant, and should be applied directly over the lacrimal sac, just under the child may only require refractive correction. Surgery the medial canthal tendon, with the small finger of the is indicated if the cataract is large enough to block vision, parent’s hand. The parent should be advised to ensure and must be performed as soon as possible to prevent closure of the eyelids so that the puncta are occluded at all amblyopia. In this way, the lacrimal sac does not the convex power of the lens has to be replaced by empty into the conjunctival sac during massage, ensuring spectacles, contact lenses or intraocular lenses. Intraocular an adequate hydrostatic pressure to push debris into lenses are not implanted in children less than 2 years of age the nose. Empirical antibiotic eye drops are prescribed to since the eyeball is yet to grow and the refractive power will prevent infection. If the ophthalmologist will perform syringing and probing they are older than 2 years at the time of surgery, intraocular (under general anesthesia) to mechanically push the debris lenses are preferred. Probing may be repeated two or three times; spectacle correction for near work as they get older. They if it fails, surgery in the form of dacryocystorhinostomy is will need intensive follow-up to manage refractive changes, indicated. If an after-cataract produce an acutely painful, erythematous swelling of the does form, the visual axis has to be cleared using laser or lacrimal sac. If the cataract is a familial abnormality, all siblings overlying skin resulting in fistula formation. Infection may and offsprings must be screened within 2 weeks of birth, spread beyond the sac to produce preseptal cellulitis, or and periodically thereafter for some years. More serious complications (cavernous sinus thrombosis, blindness and death) may supervene in immunocompromised individuals. The discharge should be cultured, and immediate broad spectrum systemic antimicrobial therapy started. Scarring from the acute event may prevent successful syringing and probing; dacryocystorhinostomy is usually indicated. Pediatricians play a vital role in diagnosing cataract since they are in a position to screen 1023 congenital Glaucoma Primary developmental glaucoma (congenital glaucoma) results when elevated intraocular pressure occurs in the first 4 years of life. The principal defect is a failure in cleavage of the anterior chamber angle during embryogenesis. The characteristic clinical picture is enlargement of the eyeball; the infant sclera is more elastic than in the adult and stretches in response to elevated intraocular pressure. The enlarged eye resembles that of the ox, and the condition is called buphthalmos (ox eye). The presenting triad is watering, photophobia and blepharospasm; these result from the large edematous cornea. In general, a horizontal corneal diameter greater than 12 mm is highly indicative of the disease. Optic disc cupping is seen early, increases rapidly and reverses to some extent with treatment. Glaucoma in childhood may be secondary to ocular developmental disorders like aniridia (congenital absence of iris), or ectopia lentis (subluxation of lens). It may also be associated with systemic syndromes (Sturge-Weber syndrome, neurofibromatosis). Children with these dis- orders should be referred for periodic examination to an ophthalmologist. Examination under anesthesia is mandatory to rule out other conditions that mimic congenital glaucoma (megalocornea, keratitis, ophthalmia neonatorum, muco- polysaccharidosis). Large corneal diameters (vertical and horizontal), optic disc cupping, characteristic corneal Chemical injuries must be urgently managed at first edema and elevated intraocular pressure clinch the diag- presentation by thoroughly washing out all chemicals using nosis. Pressure any available inert solution; tap water, saline, Ringer’s lactate must be medically controlled before surgery. Particulate material should be mechanically successful control of glaucoma, the child needs treatment removed, and washing should continue for 15 minutes, for refractive error induced in the enlarged eye and for before referral to an ophthalmic center. Follow-up must be life-long, since the effect of trauma too, the child should be referred; however, if there is surgery tends to diminish over time. The child complains of sudden onset of foreign body sen- Most occur due to unsupervised play and are preventable. While conjunctivitis can Usual modes of injury in children include stick, bow and also cause foreign body sensation, the pricking sensation arrow. Corneal foreign bodies injury may be mechanical or chemical; mechanical trauma may be immediately visible; if it is not dislodged by irrigating may result in concussion or a sharp, lacerating injury. The with normal saline (under topical anesthesia), refer to an eyelids, orbits or eyeball may be involved (s 18. Very often, there is a clear cut history of injury; palpebral conjunctiva may be removed using a sterile sometimes, particularly in preverbal children, no history cotton swab stick; one in the superior palpebral conjunctiva is given. In suspected injury, like child abuse, even if there can only be visualized and removed on everting the eyelid. Ocular injuries antibiotics should be prescribed for a few days to prevent have potential to cause loss of vision; in addition, eyelid infection. Corneal abrasion induced by the foreign body or and orbital injuries may result in disfigurement, causing by the process of its removal will necessitate padding and 1024 psychosocial morbidity as well.

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Meperidine is a phenylpiperidine generic compazine 5 mg visa symptoms lyme disease, not a phenanthrene order compazine 5 mg fast delivery medications herpes, and the active metabolite buy 5 mg compazine otc treatment vertigo, normeperidine cheap compazine 5mg amex pretreatment, is not reversible by naloxone. In most cases of buprenorphine overdose, the dose of naloxone needs to be high and continuous due to the higher binding affinity to the mu receptor. Naloxone is effective for fentanyl overdoses; however, fentanyl is a phenylpiperidine, and not a phenanthrene. She reports that the pain has been uncontrolled with tramadol, and it is decided to start treatment with an opioid. It is very important to use a low dose and monitor closely for proper pain control and adverse effects. Meperidine should not be used for chronic pain, nor should it be used in a patient with renal insufficiency. The transdermal patch is not a good option, since her pain is considered acute and she is opioid naïve. Morphine is not the best choice due to the active metabolites that can accumulate in renal insufficiency. Buprenorphine has a much higher incidence of opioid-induced respiratory depression compared to other μ agonists. Buprenorphine has many dosage formulations, and all formulations can be prescribed for the treatment of pain or opioid dependence. Buprenorphine has a lower incidence of opioid-induced respiratory depression compared to the μ agonists due to the ceiling effect created by the partial μ agonist activity. Buprenorphine is available in many different dosage formulations, but these formulations are indicated for either pain management or medication-assisted treatment of opioid dependence, not both. Based on the mechanism of action, which opioid could be considered in this patient to treat both nociceptive and neuropathic pain? Tapentadol has a unique mechanism of action in comparison with the other choices given. Tapentadol has a dual mechanism of action (μ agonist and norepinephrine reuptake inhibition), which has been shown to effectively treat neuropathic pain associated with diabetic peripheral neuropathy. All other μ agonists could help manage neuropathic pain, but in some situations, higher doses of opioids are needed to achieve efficacy. Methadone is an excellent choice for analgesia in most patients because there are limited drug–drug interactions. The duration of analgesia for methadone is much shorter than the elimination half-life. The active metabolites of methadone accumulate in patients with renal dysfunction. The duration of analgesia is much shorter than the elimination half-life, leading to dangers of accumulation and increased potential for respiratory depression and death. The equianalgesic potency of methadone is extremely variable based on many factors, and only providers familiar with methadone should prescribe this agent. The drug interactions associated with methadone are numerous due to the multiple liver enzymes that metabolize the drug. Methadone does not have active metabolites, which makes it a treatment option in patients with renal dysfunction. Which of the following is a short-acting opioid and is the best choice for this patient’s breakthrough pain? Hydrocodone is a commonly used short-acting agent that is commercially available in combination with either acetaminophen or ibuprofen. Methadone should not routinely be used for breakthrough pain due to the unique pharmacokinetics and should be reserved for practitioners who have experience with this agent and understand the variables associated with this drug. Fentanyl is available in formulations for treatment of breakthrough pain for cancer treatment. Nalbuphine is a mixed agonist/antagonist analgesic that could precipitate withdrawal in patients who are currently taking a full μ agonist such as oxycodone. Which of the following opioids would have the lowest chance of drug interactions in this patient? The risk of respiratory depression is highest during an initial opioid initiation or following a dose increase. The incidence of nausea and sedation increases with long-term use of opioid therapy. Decreased testosterone levels are commonly seen with short-term use of opioid therapy. The risk of respiratory depression is highest when the opioid is first initiated or a dosage is raised (or sometimes a drug–drug interaction leads to higher opioid levels). Opioid-induced constipation can occur at any time during the therapy, and a patient does not develop a tolerance to this side effect. Side effects such as nausea and sedation commonly decrease after repeated dosing due to development of tolerance to these adverse effects. Chronic opioid exposure has been linked to decreased testosterone levels in males. He has been converted to oral morphine in anticipation of discharge from the hospital. A bowel regimen should be prescribed with the initiation of the opioid since constipation is very common and can occur at any time, and tolerance to this adverse effect does not occur. Docusate sodium is a stool softener that is ineffective in opioid-induced constipation when used as a single agent. Combination products that include both docusate and senna are commonly used and can be effective, mainly due to the actions of senna. Diphenhydramine can be used for urticaria that might occur with the initiation of an opioid, and methylphenidate has been used for opioid-induced sedation in certain situations, but these issues are not reported in this case. His pain has been fairly well controlled, and he remains active, reports satisfaction with his pain regimen, and denies any side effects. Which of the following options is the best treatment recommendation for him at this time? Taper off all opioids due to increased risk of opioid-induced respiratory depression. Prescribe naloxone nasal spray to have at home in case he experiences an opioid overdose. Prescribe oral naloxone tablets to have at home in case he experiences an opioid overdose. Since the pain is controlled and no side effects are reported, tapering off the opioids at this time is not the best answer. Because of the first-pass effect, naloxone is not clinically effective for management of an overdose when given orally. Offering the at-home naloxone nasal spray, along with proper education, might be lifesaving if an overdose occurs. Providing proper education to the patient and caregivers on the importance of having the naloxone nasal spray at home and of calling emergency services is critical in case of an overdose situation. The psychomotor stimulants cause excitement and euphoria, decrease feelings of fatigue, and increase motor activity. The hallucinogens produce profound changes in thought patterns and mood, with little effect on the brainstem and spinal cord.

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Serum alcohol levels and a drug screen can detect potential intoxicants and prompt administration of necessary antidotes or other measures compazine 5mg overnight delivery medicine wheel. Treatment of Respiratory and Other Organ Failure the initial management of all pulmonary edema states involves monitoring PaO and providing appropriate supplemental oxygen buy 5mg compazine mastercard 5 medications post mi. However buy compazine 5mg amex medications known to cause tinnitus, because of the potential impact of hypercapnia on cerebral blood volume order compazine 5mg with amex symptoms xanax, permissive hypercapnia should not be employed without intracranial pressure monitoring in comatose drowning victims [25]. Other therapies for the respiratory complications of drowning have been proposed, but none of those has demonstrated improvements of outcomes. Examples of these types of therapies include exogenous surfactant in respiratory failure and prophylactic antibiotics. Sinus and atrial dysrhythmias as well as most interval prolongations rarely require additional therapy. For a discussion of the treatment of hypothermia-related malignant ventricular dysrhythmias, see Chapter 184. Contractures are treated with casts or splints; subluxated or dislocated hips can be approached with appropriate operative procedures; and scoliosis is treated with bracing or spinal instrumentation [27]. Neurologic Therapy the quality of the evidence supporting any intervention is poor when addressing neurologic resuscitation of the drowning victim. Therefore, much of what is recommended is based on a consensus understanding of the available information supplemented by general principles of resuscitation. The following recommendations are based on the World Congress on Drowning and more recent publications. In- water rescue may be attempted by a trained lifeguard, but untrained individuals are likely to impair their own swimming by doing so and will probably be better served by bringing the victim to land. It is not necessary to continue aggressively rewarming a drowning victim once spontaneous circulation has been recovered, unless the hypothermia is thought to be contributing to ongoing arrhythmias or other serious pathology. Hyperthermia should be prevented and normothermia maintained at all times in the acute recovery period. Therapeutic hypothermia to a core temperature of 32°C to 36°C is recommended for a period of 24 hours for comatose survivors [48,49,50]. On the other hand, patients with delayed resuscitation and those who do not rapidly recover neurologic function often have poor outcomes. Although freshwater and seawater drownings cause different clinical pictures in experimental animals, they are difficult to distinguish for human drowning victims. They usually do not aspirate enough fluid to produce changes in blood volume, electrolytes, hemoglobin, and hematocrit of sufficient magnitude to be life-threatening. These include removing wet clothing, covering with warm blankets, infusing warm fluids intravenously, and performing gastrointestinal irrigation with warm fluids. If the patient’s temperature is less than 32°C, core rewarming may be most easily accomplished by cardiopulmonary bypass or peritoneal dialysis with a potassium-free dialysate warmed to 54°C. The most important methods for reducing deaths from drowning currently reside in the area of drowning prevention. Yang L, Nong Q, Li C, et al: Risk factors for childhood drowning in rural regions of a developing country: a case–control study. Xu X, Tikuisis P, Giesbrecht G: A mathematical model for human brain cooling during cold-water near-drowning. Schwameis M, Schober A, Schorgenhofer C, et al: Asphyxia by drowning induces massive bleeding due to hyperfibrinolytic disseminated intravascular coagulation. Miki A, Takeda S, Yamamoto H, et al: A case of renal impairment after near-drowning: the universal nature of acute kidney injury. Sramek P, Simeckova M, Jansky L, et al: Human physiological responses to immersion into water of different temperatures. Rosen P, Stoto M, Harley J: the use of the Heimlich maneuver in near drowning: Institute of Medicine Report. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Hypothermia After Cardiac Arrest Study Group: Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. Inflammation of the airways causes airway obstruction by making airway smooth muscle more sensitive to contractile stimuli, by thickening the airway wall with edema and inflammatory cell infiltration, by stimulating glands to secrete mucus into the airway lumen, by damaging the airway epithelium, and by remodeling the architecture of the airways. Acute exacerbations of asthma may punctuate the course of mild, moderate, or severe cases of chronic asthma. These exacerbations or flares of asthma can be life-threatening and are characterized by an acute, progressive worsening of respiratory symptoms and pulmonary function that is severe enough to warrant a change in treatment [1]. Typically, mild-to-severe exacerbations are triggered by poor adherence to asthma controller medications or by exposure to environmental factors such as inhaled allergens, irritants, or viral infections of the respiratory tract. Assessment, management, and prevention of exacerbations of asthma, especially those leading to respiratory failure, are the critical challenges of caring for adult patients with asthma [1–3]. Worldwide, clinical asthma ranks among the most common chronic diseases, with a prevalence ranging from 1. Asthma exacerbation rates vary by season with peaks in emergency room visits and hospitalizations coinciding with respiratory viral infections, especially rhinoviral infections, in late summer and early autumn. In 2010 National Hospital Discharge Survey data, annual rates for inpatient hospital discharges for asthma in the United States were 18. Although there remain important racial and gender differences in the rates of hospitalization, there was an overall decline in hospitalizations from 1995 to 2002, possibly due to better management and prevention [6]. Asthma mortality rates also have an annual cycle but do not strictly parallel the cycle for exacerbations. Among children, mortality peaks during the summer months, but, with increasing age, asthma mortality becomes more common during the winter months [7]. Deaths among patients hospitalized for asthma do account for one-third of asthma-related mortality, but potential differences of hospital care do not appear to account for racial disparities, and this suggests that prehospitalization factors are important [8]. These findings occur in both severe and mild asthma, suggesting that airway inflammation is of primary importance in the pathogenesis of asthma. For exacerbations of asthma, the pathology of the airways is variable, reflecting at least two recognized clinical subtypes of exacerbation—slow onset and rapid onset. Slow onset exacerbations are the most common (approximately 80% of exacerbations) and the patient presents with more than 2 to 6 hours of symptoms—often days or weeks of symptoms [13–15]. This suggests that most such patients should have sufficient time to seek medical attention for worsening shortness of breath [16]. At autopsy, the lungs of patients who die of “slow-onset” asthma exacerbations are hyperinflated with thick tenacious mucus filling and obstructing the lumens of the airways. Microscopically, there is an eosinophilic bronchitis, with pronounced areas of mucosal edema and desquamation of the epithelium. Typically, hypertrophy and hyperplasia of smooth muscle are present and the muscle appears contracted [17]. The patient with the rapid-onset type of exacerbation presents with severe symptoms that have rapidly progressed over 2 to 6 hours [13–15].

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Owing to remember the disc levels generic 5mg compazine amex medicine 666 colds, exiting roots and which root is compressed is: the relative height of the • the compressed root is always the lumbar vertebral bodies cheap 5 mg compazine with mastercard treatment xanthelasma eyelid, a second number in the disc level name prolapsed lumbar disc does (e cheap compazine 5 mg without a prescription schedule 8 medications list. L2/3 disc herniation compresses not compress the nerve root root L3; C4/5 disc herniation exiting at the same level (e quality 5 mg compazine symptoms 2 year molars. Key diferential diagnoses Tone can be found to be increased or decreased: • increased tone is suggested by an ankle that appears fxed in position when the thigh is rolled or when the heel comes of the couch upon jerking the knee. It can be pathological, normal or from anxiety • reduced tone indicates decreased tonic activation of muscles. Power 113 Approach the general principles of assessing power in the upper limbs (Chapter 4) apply here too. Sequence the sequence tests the muscles in turn in a logical order to assess a number of muscles from each major peripheral nerve and nerve root. Radicular pain is weak ness in muscles inner- usually the frst symptom of nerve root vated by several peripheral compression. Typically, distal is usually indicates the level of origin: worse than proximal and it Nerve Pain radiation is usually symmetrical root • sacral plexopathies are afected C5 Shoulder essentially unilateral C6 Lateral forearm and thumb polyneuropathies with C7 Dorsum of hand and muscles affected from middle fnger multiple nerves C8 Medial forearm, medial two fngers • a root lesionis most readily L1 Groin identifed by the distribution L2 Medial thigh of pain; however, if there is L3 Knee L4 Inner calf involvement of the ventral L5 Outer calf and great toe or spinal root, weakness will S1 Lateral foot and sole also be seen. This will be in S2 Posterior thigh muscles not restricted to a single peripheral nerve but to a recognisable spinal Clinical insight level Getting above the lesion: when signs of weakness (or sensory disturbance) are What happens next? The following features suggest a cerebellar lesion: • dysmetria: overshooting the target • intention tremor: tremor beginning as the heel approaches the target • dysdiodochokinesia: disorganised movements Proprioceptive loss can also cause tremor or dysmetria but this tends to be less dramatic. Tell them that you are going to ask them whether the pin-prick is sharp or dull and to compare it between sides. The principles of the sensory examination are to: • start distally and work proximally • test each major peripheral nerve • test each major dermatome • test both lateral and dorsal columns of the spinal cord • map out any area of sensory change encountered Equipment This requires a Neurotip, tuning fork and universal containers with hot and cold water. However, if cauda equina syndrome is suspected, also ensure to check perianal and perineal sensation: 122 Lower limbs • buttocks (inferior lateral clunical nerve; S3) • perianal (pudendal nerve; S4/5) 4. For this, test: • hips (L1) • level of the umbilicus (T10) • halfway between the umbilicus and nipples (T7) • level of the nipples (T4) • lower border of the clavicle (T2) 5. For this, test: • rib at the level of the umbilicus (T10) • rib halfway between the umbilicus and nipples (T7) • rib at the level of the nipples (T4) • clavicle (T2) 6. The distribution may look like multiple peripheral nerves or nerve roots • radiculopathy:usually multiple modalities. Lesions localising to the muscles or peripheral nerves should be investigated with nerve conduction studies. Inspection Syndromes, posture, fasciculations, wasting, feet Tone Spastic, faccid Power Gluteus maximus, adductors, iliacus, quadriceps, gluteus medius/gluteus minimis, hamstrings, gastrocnemius, tibialis posterior, small muscles of the foot, tibialis anterior, extensor hallucis longus, peroneus longus and brevis Refexes Knee, crossed adductor, ankle, plantars, clonus Co-ordination Heel–shin, tap rhythm Sensation Pin-prick: (1) outer foot, great toe, medial tibia, knee, lateral thigh, popliteal fossa, buttocks, perianal, perineum; (2) thoracic region if indicated Vibration: (1) lateral malleolus, great toe, mid-tibia, tibial plateau, hip; (2) ribs and sternum if indicated Table 5. Nonetheless, a systematic approach to examining cerebellar function is needed when the history or initial examination indicates cerebellar disease. Its role in the fne control of movements is the most clinically relevant; however, it is also involved in a wide range of higher functions, including emotion and cognition. It has a unique and uniform arrangement of cells that constitute basic circuits repeated many millions of times. It can be divided into diferent regions based on gross anatomy, which also corresponds to the origin of the major inputs and outputs. The cerebellum forms the feed-forward control over movements, smoothing out movements initiated elsewhere and ensuring the intended movement is accurately performed. There are three anatomically distinct areas: the anterior lobe, the posterior lobe and the focculonodular lobe (ure 6. The cerebellum has three functionallydistinct areas, each with distinct inputs and outputs: 126 Cerebellum Spinal and trigeminal inputs Corticopontine inputs Vestibular inputs Intermediate part of hemisphere Vermis Lateral part of Anterior lobe hemisphere Fastigial nucleus Interposed nucleus Dentate nucleus Flocculondular lobe Vestibular inputs and outputs ure 6. The anatomical focculonodular lobe receives mainly vestibular inputs and projects back to the vestibular nuclei and is closely involved in eye movements. Vertigo This is the sensation of the environment spinning while stationary – like ‘stepping of a roundabout’. Patients may not be familiar with this meaning of the word, and so care should be taken to fully determine the nature of any dizziness, faintness or unsteadiness that they report. Ataxia may be evident on walking, when a patient will tend to fall to the afected side of a unilateral lesion. Similar symptoms such as dysmetria (overshooting or undershooting a target) and impaired check (failure to stop a limb movement appropriately) also commonly occur in cerebellar lesions. As with many of the clinical abnormalities of cerebellar disease, it is thought to be due to poor co-ordination of agonist and antagonist muscles. There are distinct ‘cerebellar syndromes’ comprising a constellation of these symptoms that point to a particular anatomical location of the lesion. Syndrome Location of lesion Predominant clinical features Rostral vermis Anterior lobe/rostral Broad-based gait syndrome vermis Truncal ataxia Caudal vermis Posterior or Vertigo syndrome focculonodular lobe Staggering gait Truncal ataxia Nystagmus Hemispheric Cerebellar hemisphere Limb ataxia syndrome Intention tremor Dysmetria Dysarthria Dysdiodokokinesia Table 6. Lesions of the vermis tend to cause more truncal ataxia than limb ataxia, and fewer obvious limb signs. Lesions in the hemispheres cause a greater range of symptoms and include prominent limb signs ipsilateral to the lesion 132 Cerebellum Cerebellar disease has many underlying causes, both de- velopmental/hereditary and acquired. Developmental or hereditary Key causes include Arnold–Chiari and Dandy–Walker malforma- tions and the hereditary ataxias. The hereditary ataxias These include a large number of rare autosomal dominant and recessive conditions: • the most common autosomal dominant conditions are the spinocerebellar ataxias, which are chronic, progressive conditions. There is often arefexia of the ankles, cardiomyopathy and diabetes in up to one-quarter of cases Acquired There are a wide range of acquired causes of cerebellar disease, including vascular, toxic, neoplastic, infective and autoimmune pathologies. This causes headache in addition to cerebellar symptoms and commonly causes decreased consciousness and may lead to life-threateninghydrocephalus Toxins Alcohol is the most common toxic cause. Chronic overuse can lead to Wernicke’s (ataxia, acute confusion, eye movement disorder) or Korsakoff’s syndromes (a chronic amnesic state). Benzodiazepines, phenytoin, carbamazepine, chemo- therapeutic drugs and lithium are the more common drugs associated with dysarthria and ataxia. Tumours In children medulloblastomas, astrocytomas and ependy momasare relatively common primary tumours found in the cerebellum. Paraneoplastic syndromescausing cerebellar syn- dromes are well described and are usually the result of small cell lung carcinoma or breast cancer. Infective or immune There are many infective or immune causes, including: • encephalitis from any cause can result in an initial cerebellar syndrome but usually progresses to a more forid encephalitic picture • autoimmune diseases such as multiple sclerosisare a common cause in young people and are typically of a subacute nature • up to 10% of patients with coeliac diseasehave neurological involvement and this can include a slowly progressive cerebellar syndrome What happens next? Patients with cerebellar disease not readily explained by vascular causes or alcohol usually require careful and extensive investigation. Revisiting the family history is an ideal place to start and it may be helpful to actually see and examine family members. General observation Inspect body and feet Palpate pulse, auscultate carotids Palpate abdomen Vertigo Ataxia Sitting Standing Walking Nystagmus Primary gaze Gaze evoked Intention tremor Reassess with fnger–nose test Test for impaired check Speech Note any dysarthria or scanning speech Hypotonia Assess tone in limbs Dysdiodochokinesia Test alternating clapping Test heel–shin. Although it is less useful for fne localisation, it is very helpful in determining the impact of a disease process on a patient’s cognitive processes and for assessing its progression over time. This is often all that is needed in patients without significant cognitive impairment and provides an assessment of: • orientation Clinical insight • registration (immediate memory) Patients vary greatly in their background education and cultures. It is also more reliable at distinguishing between diferent subtypes or dementia, such as Alzheimer’s disease, frontotemporal dementia and supranuclear palsy. Bedside cognitive examinations are not designed to tease out precise anatomical regions; language function is the exception, and is discussed below. Language Language is such a defning feature of our human nature that the complexity of neural computations that it requires is easily overlooked.

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