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The story makes for a good ward round anecdote generic detrol 4 mg without prescription, and I could leave matters there discount detrol 1mg overnight delivery. I could be working with this radiologist for the rest of my pro- fessional life 4 mg detrol overnight delivery. After all buy detrol 4mg amex, the problem on one level is merely about good manners and common courtesy purchase 4mg detrol free shipping. You need to know the following information before going to discuss anything with a radiographer or radiologist and be able to present it in a con- cise and logical order. Radiologists and Radiographers 51 3 When – is it an emergency or urgent or routine investigation? Lastly, after you have supplied the information to the radiologist, if the request is accepted you then need to ask some questions of the radiologist. Radiological Procedures: What Information Is Required and What to Do The difference between an investigation and a procedure is that one is non-invasive and one is invasive, respectively. Investigations usually require minimal input from the jun- ior doctor and once the investigation is performed the patient goes back to the ward and needs minimal extra care. In contrast, a radiological procedure can produce significant extra work and the patient may require much more care before and after the event. Used for examining blood vessels (for example, an intra-arterial digital 52 What They Didn’t Teach You at Medical School subtraction angiogram (IADSA)) and the bowel (barium meal, follow-through or enema). For care of patients after radiological procedures you can follow the outlines listed above in the section on some questions to ask the radiologist, but you will need to supplement your plan of care by asking more experienced ward-based staff such as your specialist registrar (SpR) and senior nurses. The very best example of this inter- action can be found on a vascular surgery ward where these types of procedures are performed on many patients on a daily basis. Often integrated care pathways are in place to make sure all patients are well monitored. Specialist Radiology Traditionally the term ‘specialist radiology’ has been applied to most radiological investigations not using traditional methods, that is X-rays for producing radio- graphs. However, with the introduction of more and more technology, CT and MRI scanning has become part and parcel of everyday radiology and specialist examin- ations are now considered those investigations that are required to be performed by radiologists that have specialised in a particular field. Some of these investigations use radioisotopes and are performed in a separate department called nuclear medi- cine (also colloquially referred to as unclear medicine, usually because most doctors are unable to read the scans themselves and require a radiologist to write a report). The best example is a bone scan to determine the presence of bony metastasis from a primary tumour. Others include scintimammograms (99Te), scintiangiography (used for deter- mining organ function based on the distribution of the blood supply, for example a thallium scan for cardiac function), renal scanning (mercaptoacetylglycine (MAG-3), dimercaptosuccinic acid (DMSA) or diethylene triamine penta-acetic acid (DTPA)) and bone scans. Particularly useful for looking at the mediastinum, which is inaccessible to biopsy. Specialist radiological procedures can be tricky to organise, not because the radiolo- gists are difficult to corner, but usually because the request forms are difficult to find Radiologists and Radiographers 53 unless you are based on a specialist ward. The easiest way to find forms is to go to the relevant ward and ask a staff nurse to tell you where they are kept. Make sure you introduce yourself first or are wearing hospital identification otherwise you will not be given one. If that fails then telephone the department (which may not even be located in your hospital: this is particularly true of PET) and ask their receptionist’s advice. Often you may have to type out a referral and fax it to the relevant depart- ment. If you are still at a loss then telephone the senior house officer in that special- ity, for example vascular, breast, etc. You may find that they offer to request it for you, as they know the system so have the details to hand. Make sure you try the other avenues first as they will be sure to ask you and will not be impressed if you have not shown initiative. This fancy title encompasses some of the most important people you will work with, who not only make a huge difference to your patients, but will make your life easier as they help to get your patients home. Often doctors, who are ignorant of what they do, do not give these highly skilled individuals the respect they really deserve. Now, as a qualified doctor I interact with them every day and notice that other doctors who ignore them are those who do not get on with nurses or their patients either. As an undergraduate I really had no concept of what these people did until I had to spend two days with them as part of my senior curriculum. If you are sociable and want to do the best for your patients then read on...

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British Journal of General Practice 1996; 46: 743-747 Cross References Bell’s phenomenon buy generic detrol 1 mg line, Bell’s sign; Facial paresis; Lower motor neurone (LMN) syndrome Bell’s Phenomenon detrol 1 mg generic, Bell’s Sign Bell’s phenomenon or sign is reflex upward purchase 2mg detrol with amex, and slightly outward order 2mg detrol amex, devi- ation of the eyes in response to forced closure cheap detrol 2 mg with mastercard, or attempted closure, of the eyelids. This is a synkinesis of central origin involving superior rectus and inferior oblique muscles. It may be very evident in a patient with Bell’s palsy (idiopathic facial nerve paralysis) attempting to close the paretic eye- lid. The reflex indicates intact nuclear and infranuclear mechanisms of upward gaze, and hence that any defect of upgaze is supranuclear. However, in making this interpretation it should be remembered that per- haps 10-15% of the normal population do not show a Bell’s phenomenon. Bell’s phenomenon is usually absent in progressive supranuclear palsy and is only sometimes spared in Parinaud’s syndrome References Bell C. On the motions of the eye, in illustration of the use of the muscles and nerves of the orbit. Philosophical Transactions of the Royal Society, London 1823; 113: 166-186. Cross References Bell’s palsy; Gaze palsy; Parinaud’s syndrome; Supranuclear gaze palsy; Synkinesia, synkinesis Benediction Hand Median nerve lesions in the axilla or upper arm cause weakness in all median nerve innervated muscles, including flexor digitorum profun- dus. On attempting to make a fist, impaired flexion of the index and middle fingers, complete and partial respectively, results in a hand pos- ture likened to that of a priest saying benediction. A somewhat similar, but not identical, appearance may occur with ulnar nerve lesions: hyperextension of the metacarpophalangeal joints - 54 - Blepharospasm B of the ring and little fingers with slight flexion at the interphalangeal joints. The index and middle fingers are less affected because of the intact innervation of their lumbrical muscles (median nerve). Cross References Claw hand; Simian hand Bent Spine Syndrome - see CAMPTOCORMIA Bielschowsky’s Sign, Bielschowsky’s Test Bielschowsky’s sign is head tilt toward the shoulder, typically toward the side contralateral to a trochlear (IV) nerve palsy. The intorsion of the unaffected eye brought about by the head tilt compensates for the double vision caused by the unopposed extorsion of the affected eye. Bielschowsky’s (head tilt) test consists of the examiner tipping the patient’s head from shoulder to shoulder to see if this improves or exacerbates double vision, as will be the case when the head is respec- tively tilted away from or toward the affected side in a unilateral trochlear (IV) nerve lesion. The test is usually negative in a skew devi- ation causing vertical divergence of the eyes. This test may also be used as part of the assessment of vertical diplopia to see whether hyper- tropia changes with head tilt to left or right; increased hypertropia on left head tilt suggests a weak intortor of the left eye (superior rectus); increased hypertropia on right head tilt suggests a weak intortor of the right eye (superior oblique). Cross References Diplopia; Hypertropia; Skew deviation Bitemporal Hemianopia - see HEMIANOPIA; VISUAL FIELD DEFECTS Blepharoptosis - see PTOSIS Blepharospasm Blepharospasm is a focal dystonia of the orbicularis oculi resulting in repeated involuntary forced eyelid closure, with failure of voluntary opening. The condition typically begins in the sixth decade of life, and is com- moner in women than men. Blepharospasm may occur in isolation or in combination with other involuntary movements which may be dys- tonic (orobuccolingual dystonia or Meige syndrome; limb dystonia) or dyspraxic (eyelid apraxia). Blepharospasm is usually idiopathic but may be associated with lesions (usually infarction) of the rostral brainstem, diencephalon, and striatum; it has been occasionally reported with thalamic lesions. The - 55 - B Blind Spot pathophysiological mechanisms underlying blepharospasm are not understood, but may reflect dopaminergic pathway disruption causing disinhibition of brainstem reflexes. Local injections of botulinum toxin into orbicularis oculi are the treatment of choice, the majority of patients deriving benefit and requesting further injection. Failure to respond to botulinum toxin may be due to concurrent eyelid apraxia or dopaminergic therapy with levodopa. Journal of Neurology, Neurosurgery and Psychiatry 1988; 51: 767-772 Hallett M, Daroff RB. Neurology 1996; 46: 1213-1218 Cross References Blinking; Dystonia; Eyelid apraxia; Gaping; Yawning Blind Spot The blind spot is defined anatomically as the point on the retina at which axons from the retinal ganglion cells enter the optic nerve; since this area is devoid of photoreceptors there is a physiological blind spot. This area may be mapped clinically by confrontation with the examiner’s blind spot, or mechanically. Enlargement of the blind spot (peripapillary scotoma) is observed with raised intracranial pressure causing papilledema: this may be helpful in differentiating papilledema from other causes of disc swelling, such as optic neuritis, in which a central scotoma is the most common field defect. Enlargement of the blind spot may also be a feature of peripapillary retinal disorders including big blind spot syndrome. Cross References Disc swelling; Papilledema; Scotoma Blinking Involuntary blinking rate is decreased in idiopathic Parkinson’s disease (and may be improved by dopaminergic therapy) and progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome). In contrast, blink rate is normal in multiple system atrophy and dopa-responsive dys- tonia, and increased in schizophrenia and postencephalitic parkinsonism. These disparate observations are not easily reconciled with the suggestion that blinking might be a marker of central dopaminergic activity. In patients with impaired consciousness, the presence of invol- untary blinking implies an intact pontine reticular formation; absence suggests structural or metabolic dysfunction of the reticular forma- tion.

CIDP may manifest with a chronic progressive cheap 4mg detrol amex, monophasic detrol 1 mg free shipping, or relapsing–remitting clinical course detrol 1 mg. Weakness is primarily a consequence of conduc- tion block resulting from focal demyelination; as such it often responds well to treat- ment proven 1mg detrol. After years of disease order 2mg detrol free shipping, there can be accumulating axonal degeneration, clinically evident by wasted muscles, which may be irreverisible. There are many causes of symmetrical weakness in children ranging from central nervous system disorders to muscle disease. In patients without sensory symptoms and signs, anterior horn cell disease (spinal muscular atrophy), neuromus- cular junction disease, and muscle disease are important considerations. Neuropathy in children is often due to inherited disorders such as Charcot-Marie-Tooth disease (CMT type 1–4 and X) or less commonly due to inborn errors of metabolism such as Krabbe’s disease, metachromatic leukodystrophy, Refsum’s disease, adrenomyelo- leukodystrophy, or acute intermittent porphyria. A diagnosis of CIDP is made primarily on the basis of nerve conduction studies (Table 4). Although decreased conduction velocities and prolonged distal motor latencies can be seen in both CIDP and hereditary demyelinating neuropathy, CIDP is distinguished by the presence of 172 Sumner Table 4 Clinical and Electrophysiologic Criteria for Childhood CIDP Mandatory clinical criteria Progression of muscle weakness in proximal and distal muscles of upper and lower extremities over at least 4 weeks, or rapid progression (GBS-like presentation) followed by a relapsing or protracted course (>1 year) Major laboratory features Electrophysiologic criteria Must demonstrate at least three of the following four major abnormalities in motor nerves (or two of the major plus two of the supportive criteria) A. Conduction block or abnormal temporal dispersion in one or more motor nerves at sites not prone to compression: a. Conduction block: at least 50% drop in negative peak area or peak-to-peak amplitude of proximal compound action potential (CMAP) if duration of negative peak of proximal CMAP is < 130% of distal CMAP duration. Temporal dispersion: abnormal if duration of negative peak of proximal CMAP is > 130% of distal CMAP duration. Reduction in conduction velocity (CV) in two or more nerves: <75% mean of mean CV value for age minus 2 standard deviations (SD). Prolonged distal latency (DL) in two or more nerves: >130% of mean DL value for age þ2SD. Absent F-waves or prolonged F-wave minimal latency (ML) in two or more nerves: >130% of mean F-wave ML for age þ 2SD. Supportive When conduction block is absent, the following abnormal electrophysiological parameters are indicative of nonuniform slowing and thus of acquired neuropathy: 1. Abnormal median sensory nerve action potential (SNAP) while sural nerve SNAP is normal. Abnormally low terminal latency index: distal conduction distance (mm)= (conduction velocity [m=sec]) Â distal motor latency [msec]). Side-to-side comparison of motor CVs showing a difference of >10 m=sec between nerves. Cerebrospinal fluid (CSF) criteria Protein > 45mg=dL Cell count <10 cells=mm3 Nerve biopsy features Predominant features of demyelination Exclusion criteria A. Clinical features of history of a hereditary neuropathy, other disease, or exposure to drugs or toxins known to cause peripheral neuropathy. Laboratory findings (including nerve biopsy or genetic testing) that show evidence of a cause other than CIDP. Electrodiagnostic features of abnormal neuromuscular transmission, myopathy, or anterior horn cell disease. Inflammatory Neuropathies: GBS and CIDP 173 Figure 1 Proposed treatment algorithm for childhood chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). A nerve biopsy is sometimes diagnos- tic, but not necessary and now not routinely done. An elevated CSF protein without pleocytosis is evident in at least 90% of children with CIDP. Magnetic resonance imaging can show gadolinium enhancement of nerve roots that favors a diagnosis of CIDP over CMT. Therapy The two most commonly used immunomodulatory therapies for children with CIDP are oral corticosteroids and IVIg. A detailed discussion needs to be undertaken with the patient and family to explain the rationale for treatment and the potential short- and long-term side effects. IVIg has been shown to be effective in clinical trials in adult patients. The reported experience in small case series of children also supports its use in this age group. Prednisone has been used for many years in childhood CIDP and reported to be effective in several case series. Unfortunately, there are many poten- tial side effects of prednisone including weight gain, hyperglycemia, neuropsychiatric disturbance, impaired wound healing, avascular hip necrosis, hyperlipproteinemia, accelerated atherosclerosis, osteoporosis, myopathy, peptic ulcer disease, and cataracts. In some cases intermittent high dose solumedrol infusions, weaning on interval rather than dose, may have enhanced efficacy without the same degree of Cushingoid side effects.

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