Tomas Aragon MD, DrPH

• Faculty Headshot for Tomas Aragon
• Assistant Adjunct Professor
• Epidemiology
• Health Officer City & County of San Francisco
• Director Population Health Division, San Francisco Department of Public Health

https://publichealth.berkeley.edu/people/tomas-aragon/

Seizures and psychogenic attacks are the main differential diagnoses that must be considered hair loss in male guinea pigs purchase 0.5mg dutas fast delivery. The importance of establishing the mechanism of the syncopal attack has received attention (14) and the authors draw attention to the variability in diagnosis and management of syncope with the implications for reduced quality of life and excess costs hair loss cure kennel buy discount dutas. Well-developed pathways with dedicated units and experienced clinicians are needed to manage these patients hair loss in men wear purchase dutas overnight. Given the variability in the prevalence of syncope hair loss cure by quran discount dutas 0.5 mg without prescription, being dependent on the population being studied hair loss in men 50s hairstyles buy discount dutas 0.5mg line, there are difficulties in determining accurately the incidence of psychogenic attacks hair loss in men 0f purchase 0.5 mg dutas. This is more difficult given the importance of psychological factors in contributing to syncopal events, and the recognition that syncope and psychogenic attacks can co-exist in the same patient. This makes accurate assessment of incidence and prevalence of psychogenic attacks difficult. This reflects the populations being studied and the importance of detailed history taking and assessment in this population. This means that when the system is working, there is flow during both systole and diastole. When resistance to flow rises, the effects are initially seen with a reduction in diastolic flow. Intracranial pressures are influenced by venous pressures, tissue pressures, and the tendency for vessel walls to collapse. While supine, it is largely by the jugular veins, while upright it is via the vertebral complex (34,35). Raised central venous pressures due to obstructive disease or during valsalva manoeuvres. Tissue pressures can be significant because the skull is a rigid limit on space for brain expansion as is seen with tumours or bleeding. Sympathetic innervation is associated with vasoconstriction of larger vessels, but this is compensated by cerebral autoregulation with downstream vasodilation (37), so there is no net change in flow. While this has been shown in mammals, it has not been specifically shown in humans. Sensory fibres are associated with modulating cerebral blood flow and can be associated with increased blood flow as is seen in cortical spreading depression (39), seizures (40), and reactive hyperaemia (41). Hypercapnia and hypoxaemia of the cerebral circulation are both potent vasodilators of cerebral blood vessels, although the precise mechanisms may vary between the two (49,50). In terms of syncope, the regulation of cerebral blood flow by large arteries compensating for steal type phenomena is of particular interest (51,52). Clinical approach to syncope the approach to syncope varies depending on the circumstances where the patient is seen, such as the emergency department, outpatients, short stay wards in hospital, and geriatric departments. The underlying theme is to establish whether this discrete event represents a disruption in normal brain electrical activity, cerebral perfusion, a psychological functioning, a combination of any of the preceding, or something altogether different, such as primary cardiac disease or a sleep-related disorder. The index event should be described by the patient who will often be able to describe the pre-event circumstances, symptoms leading up to the loss of awareness and post-event symptoms. Any eye-witnesses should be interrogated to cover the same period and they should be encouraged to act out what they have seen, despite the potential for embarrassment for both eye-witness and patient. Identifying the eye-witness is also useful in case the history needs to be reviewed in the future and establishing their experience in assessing episodic behavioural events. If there is any photographic evidence such as a home video, it should be examined. This last aspect is invaluable for recurrent attacks and it forms an essential component of the clinical assessment of patients with recurrent attacks. There are two arms to the process, the afferent and the efferent, with the brainstem acting as the integrating mechanism. The ultimate mechanism for all syncope is loss of arterial pressure due to either failure of entry of blood into the circulation or loss of peripheral resistance. Phase 1 immediately following tilt is a period of stability with reduced cardiac vagal tone and increased peripheral resistance. Furthermore, baroreflex sensitivity has been shown to decrease in subjects undergoing orthostasis (53,56). This is not always shown when other methods are used, such as neck suction and blood volume manipulation (57). Despite this, the consistent finding of reduced baroreflex sensitivity with orthostasis alone suggests that in this posture, bipedal animals such as humans are physiologically under stress. Any further contributors to that stress will therefore tend to bring on symptoms when in that posture. Appearance (for example, whether eyes were open or shut) and colour of the person during the event. Presence or absence of movement during the event (for example, limb-jerking and its duration). With this basic information it is possible to send the patient down the most appropriate initial pathway. If there are features of neurocardiogenic syncope then they should be reviewed through primary care. If there are features of seizure then they should be assessed through the epilepsy service or the first seizure service. Syncope: singular or repeated While a single episode of syncope can be the presentation for significant disease particularly cardiac, it may not reach medical attention. It is repeated events, particularly if associated with injury that will bring patients to medical attention consistently. Where there is doubt as to the nature of the events, then an attempt to trigger an event is often necessary. A balance must be struck between sensitivity and specificity for the induced event being clinically relevant. The components include cardiac vagal control, cardiac sympathetic, vascular sympathetic, and splanchnic sympathetic control. These simple measures enable one to approach the complexities of cardiovascular autonomic regulation systematically. The manoeuvres used include carotid stimulation to assess cardiac vagal and baroreflex blood pressure responses, the effects of hyperventilation on cardiac vagal control, the act of standing and remaining standing for a period of time. It can also be used to assess the splanchnic vascular response to reduced cardiac filling (59). Furthermore, pressor responses can be elicited by isometric grip, mental arithmetic and cold stimulation (60). Management There is a perception in clinical medicine that a syncopal event is not as serious as an epileptic seizure and perhaps this reflects a widespread neurophobia in clinical medicine (62). This dichotomy may be partly a reflection of the literature, an essentially benign prognosis suggesting that there is less to be concerned about (63), while patient perceptions of the impact of recurrent episodes of loss of consciousness may not be fully taken into account (64). While some of these restrictions are external, such as driving restrictions, many more are self- or family-imposed. This is particularly so in the older population where concerns relating to the effects of falling are particularly acute and severe (12). Despite the commonest final common pathway for syncope being neurocardiogenic in origin, determining the best treatment for an individual remains challenging. Precise characterization of the cause remains the most important step for deciding on a management pathway. This largely means determining if it is a primary cardiac process and treating according to the best guidelines. The second group to consider is the group with pyschogenic attacks, which largely correspond to the hypomotor form of non-epileptic attack disorder. The third, and numerically largest group, are those with neurocardiogenic syncope. A fourth and often overlooked group are those with mixed attacks, most frequently neurocardiogenic and psychogenic attacks. Amongst this population, numbers are difficult to establish, but they were under-recognized for some time in the epilepsy population with up to 60% of patients having psychogenic attacks in addition to epileptic attacks (65). Furthermore, patients with panic attacks can hyperventilate and this can lead to secondary syncope, making it difficult to disentangle the primary process. The general approach is to determine if there is a fixed deficit in autonomic regulation. This requires assessing autonomic function, while resting after the body has established a steady state and then during a series of manoeuvres. This information is useful, but does not provide any great detail on the different components of cardiovascular autonomic control. The laboratories are expensive to maintain and need dedicated well trained staff to carry out investigations in a reproducible manner in a controlled environment. Neuroscience centres have well-developed physiology departments, which have well trained staff used to reproducibly performing physiological tests on patients. This is an ideal environment to develop physiological assessment of autonomic function in close collaboration with cardiology departments. The approach to assessment of autonomic function Within the autonomic laboratory, it is necessary to assess cardiorespiratory parameters at rest and during certain manoeuvres. The importance of exercise lies in improved aerobic fitness, blood volume, increased heart size, and quality of life (67). The role for medication is less clear though has an established a role in symptomatic treatment in preparation for longer-term lifestyle and dietary changes. Such agents can include fludrocortisone, and the sympathomimetic midodrine, though there are anecdotal reports that other medications can be helpful including serotonin re-uptake inhibitors, bisoprolol, pyridostigmine, and ivabradine. Thereafter, the management question hinges on the number and frequency of attacks. Clinical interpretation of physiology It is the approach to untangling the multiple potential causes for syncope that is key to using neurophysiology in the most efficient manner. If a rhythm disturbance is suspected, then monitoring cardiac rhythms is the way forward. If the frequency is less than twice a week, give serious thought to an implantable device to identify any serious arrhythmia. If neurocardiogenic syncope is the likely diagnosis, procedures to trigger an episode of syncope with neurophysiological monitoring are undertaken. There are a number of protocols in use around the world in different laboratories. The other component of neurophysiological assessment is to establish whether there is evidence of autonomic failure, which may be affecting the cardiovascular system. In this, the diagnosis of autonomic failure is not based on a single abnormal parameter, but the failure of multiple parameters. These parameters are a set of special manoeuvres set out in this statement and which include isometric exercise, deep breathing, carotid massage, response to standing, and the valsalva breath. How extensive the investigations are depends on the experience of both the referring clinicians and the laboratory serving them. Epidemiology of syncope/collapse in younger and older Western patient populations. A comparison of self-reported quality of life between patients with epilepsy and neurocardiogenic syncope. The relation between age, sex, comorbidity, and pharmacotherapy and the risk of syncope: a Danish nationwide study. Risk stratification in emergency department syncope patients Targeted management the most effective way of managing syncope is being able to direct specific treatments at the disability. Vasovagal syncope in the older person: differences in presentation between older and younger patients. Psychogenic nonepileptic seizure manifestations reported by patients and witnesses. Prodrome and characteristics of young and old patients presenting with vasovagal syncope to a teaching hospital. Quality of life within one year following presentation after transient loss of consciousness. Human cerebral venous outflow pathway depends on posture and central venous pressure. Effects of sympathetic stimulation and changes in arterial pressure on segmental resistance of cerebral vessels in rabbits and cats. Vascular release of superoxide radicals is enhanced in hypercholesterolemic rabbits. Calcitonin gene-related peptide promotes cerebrovascular dilation during cortical spreading depression in rabbits. Trigeminovascular fibers increase blood flow in cortical gray matter by axon reflex-like mechanisms during acute severe hypertension or seizures. Postocclusive cerebral hyperemia is markedly attenuated by chronic trigeminal ganglionectomy. Nitric oxide mediates vasodilatation in response to activation of N-methyl-D-aspartate receptors in brain.

A search for a patent foramen ovale hair loss in men explain buy dutas cheap online, which is present in 15% to 20% of normal subjects hair loss cure quick discount dutas 0.5 mg, is initially performed hair loss 4 year old dutas 0.5 mg cheap. However hair loss nutrients discount dutas 0.5 mg amex, the usefulness of transesophageal echocardiography is limited by the fact that the probe obstructs the fluoroscopic field hair loss in men zip up boots dutas 0.5mg generic,and it is impractical in the nonanesthetized patient hair loss cure 10 years generic dutas 0.5mg visa. Venous access is obtained via the femoral vein, preferably the right femoral vein because it is closer to the operator. The guidewire is then withdrawn, thus leaving the sheath and its dilator locked in place. The Brockenbrough needle comes prepackaged with an inner stylet, which may be left in place to protect it as it is advanced within the sheath. Alternatively, the inner stylet may be removed and the needle connected to a pressure transducer line (pressure monitoring through the Brockenbrough needle will be required during the transseptal puncture); continuous flushing through the Brockenbrough needle is used while advancing the needle into the dilator. A third approach, when the use of contrast injection is planned, is to attach the Brockenbrough needle to a standard three-way stopcock via a freely rotating adapter. A 10-mL syringe filled with radiopaque contrast is attached to the other end of the stopcock while a pressure transducer line is attached to the third stopcock valve for continuous pressure monitoring. The entire apparatus should be vigorously flushed to ensure that no air bubbles are present within the circuit. The Brockenbrough needle is advanced into the dilator until the needle tip is within 1 to 2 cm of the dilator tip. The needle tip must be kept within the dilator at all times, except during actual septal puncture. The curves of the dilator, sheath, and needle should be aligned so that they are all in agreement and not contradicting each other. A third abrupt leftward movement ("jump") below the aortic root indicates passage over the limbus into the fossa ovalis. The sheath and dilator assembly should never be advanced without the guidewire at any point during the procedure. Several fluoroscopic markers are used to confirm the position of the dilator tip at the fossa ovalis. As noted, an abrupt leftward movement (jump) of the dilator tip below the aortic knob is observed as the tip passes under the muscular atrial septum onto the fossa ovalis (see Video 4). Another method that can be used to ensure that the tip is against the fossa ovalis is injection of 3 to 5 mL of radiopaque contrast through the Brockenbrough needle to visualize the interatrial septum. The needle tip then can be seen tenting the fossa ovalis membrane with small movements of the entire transseptal apparatus. Typically, septal staining remains visible after contrast injection, which allows for real-time septal visualization while monitoring the pressure during transseptal puncture. If excessive force is applied without a palpable "pop" to the fossa, then the Brockenbrough needle likely is not in proper position. Absence of a pressure wave recording can indicate needle passage into the pericardial space or sliding up and not puncturing through the atrial septum. A second method is injection of contrast through the needle to assess the position of the needle tip. If the guidewire cannot be advanced beyond the fluoroscopic border of the heart, pericardial puncture should be suspected. In addition, aortic puncture should be suspected if the guidewire seems to follow the course of the aorta. In these situations, contrast should be injected to assess the position of the Brockenbrough needle before advancing the transseptal dilator. The sheath should be aspirated until blood appears without further bubbles; this usually requires aspiration of approximately 5 mL. The sheath is then flushed with heparinized saline at a flow rate of 3 mL/min during the entire procedure. When two transseptal accesses are required, the second access can be obtained through a separate transseptal puncture performed in a fashion similar to that described for the first puncture. Once the tip of the dilator falls into the fossa ovalis, gentle manipulation of the assembly under biplane fluoroscopy guidance is performed until the dilator tip passes along the guidewire through the existing transseptal puncture, without advancing the needle through the dilator. The catheter has a four-way steerable tip (160-degree anteroposterior or left-right deflections). It has a single rotating crystal ultrasound transducer that images circumferentially for 360 degrees in the horizontal plane. Gradual clockwise rotation of a straight catheter from the home view allows sequential visualization of the aortic root and the pulmonary artery. Alternatively, electrosurgical cautery (set to 15 to 20 W for a 1- to 2-second pulse of cut-mode cautery) is applied to the proximal hub of the needle as its tip is advanced out of the dilator. Importantly, the cautery should be initiated on the needle handle prior to pushing the needle tip beyond the dilator tip to help minimize the power needed to puncture the septum, and it should be stopped as soon as the needle is pushed out fully. Nonetheless, the powered needle can potentially be more traumatic at the puncture site than a standard needle, and it is possible that the transseptal puncture site created with a powered needle is less likely to close spontaneously. Similarly, inadvertent cardiac perforation occurring in the setting of powered needles can potentially be associated with greater consequences. Because of its stiffness and large caliber, the transseptal dilator should never be advanced until the position of the Brockenbrough needle is confirmed with confidence. Advancing the dilator and sheath assembly into the aorta can lead to catastrophic consequences. It is important to recognize that successful atrial septal puncture is a painless procedure for the patient. If the patient experiences significant discomfort, careful assessment should be made of the catheter and sheath locations (pericardial space, aorta). To avoid air embolism, catheters must be advanced and withdrawn slowly so as not to introduce air into the assembly. Sheaths must be aspirated with a syringe on a stopcock to the amount of their volume. Administration of heparin before, rather than after, the atrial septal puncture can also help reduce thromboembolism. Additionally, caution 4 should be used in the setting of the presence cardiac or thoracic malformation. Transseptal catheterization is feasible and safe in most patients with atrial septal defect or patent foramen ovale repair. Nonetheless, because of the altered anatomical landmarks after repair, fluoroscopic guidance for transseptal puncture can be unreliable, and the procedure can be challenging. In patients with atrial septal defect closure devices, puncture is preferably performed at the portion of the septum located inferior and posterior to the closure device and not through the device itself. In patients with a septal stitch or pericardial or Dacron patch, puncture can be achieved through the thickened septum or the patch. However, transseptal access is typically not achievable through a Gore-Tex patch (W. Cardiac electrograms are generated by the potential (voltage) differences recorded at two recording electrodes during the cardiac cycle. All clinical electrogram recordings are differential recordings from one source that is connected to the anodal (positive) input of the recording amplifier and a second source that is connected to the cathodal (negative) input. Analog systems have largely been replaced by digital recording systems that use an analog to digital (A/D) converter that converts the amplitude of the potential recorded at each point in time to a number that is stored. The most common digital recording systems sample the signal approximately every 1 millisecond. However, higher sampling frequencies can be required for high-quality recording of high-frequency, rapid potentials that can originate from the Purkinje system or areas of infarction. The faster sampling places greater demands on the computer processor and increases the size of the stored data files. In normal homogeneous tissue, the maximum negative slope (dV/dt) of the signal coincides with the arrival of the depolarization wavefront directly beneath the electrode, because the maximal negative dV/dt corresponds to the maximum sodium (Na+) channel conductance;. Therefore, a wavefront of depolarization traveling past a unipolar electrode results in a biphasic electrogram (positive then negative) representing the approach and recession of the activation wavefront. The major disadvantage of unipolar recordings is that they contain substantial far-field signals generated by depolarization of tissue remote from the recording electrode, because the unipolar electrode records a potential difference between widely spaced electrodes. Filtering the unipolar electrograms can help eliminate far-field signals; however, the filtered unipolar recordings lose the ability to provide directional information. At each point in time, the potential generated is the sum of the potential from the positive input and the potential at the negative input. The potential at the negative input is inverted; this is subtracted from the potential at the positive input so that the final recording is the difference between the two. The bipolar electrogram is simply the difference between the two unipolar electrograms recorded at the two poles. Because the far-field signal is similar at each instant in time, it is largely subtracted out, thus leaving the local signal. Therefore, compared with unipolar recordings, bipolar recordings provide an improved signal-to-noise ratio, and high-frequency components are more accurately seen. Several factors can affect bipolar electrogram amplitude and width, including conduction velocity (the greater the velocity, the higher the peak amplitude of the filtered bipolar electrogram), the mass of the activated tissue, the distance between the electrode and the propagating wavefront, the direction of propagation relative to the bipoles, the interelectrode distance, the amplifier gain, and other signal-processing techniques that can introduce artifacts. To acquire true local electrical activity, a bipolar electrogram with an interelectrode distance of less than 1 cm is desirable. Moreover, bipolar recordings do not allow simultaneous pacing and recording from the same location. To pace and record simultaneously in bipolar fashion at endocardial sites as close together as possible, electrodes 1 and 3 of the quadripolar mapping catheter are used for bipolar pacing, and electrodes 2 and 4 are used for recording. Intracardiac electrograms are usually filtered to eliminate far-field noise, typically at 30 to 500 Hz. The high-pass filter allows frequencies higher 4 than a certain limit to remain in the signal. High-Pass Filtering High-pass filtering attenuates frequencies slower than the specified cutoff (corner frequency) of the filter. If intracardiac recordings were not filtered, the signal would wander up and down as this potential fluctuated with respiration, catheter movement, and variable catheter contact. For bipolar electrograms, high-pass filters with corner frequencies between 10 and 50 Hz are commonly used. In general, high-pass filtering can be viewed as differentiating the signal, so that the height of the signal is proportional to the rate of change of the signal, rather than only the amplitude. However, filtering the unipolar signal does not affect its usefulness as a measure of the local activation time. This approach is useful for reducing high-frequency noise without substantially affecting electrograms recorded with clinical systems because most of the signal content is lower than 300 Hz. As the wavefront reaches the electrode and propagates away, the deflection sweeps steeply negative. This rapid reversal constitutes the intrinsic deflection of the electrogram and represents the timing of the most local event. The maximum negative slope (dV/dt) of the signal coincides with the arrival of the depolarization wavefront directly beneath the electrode. The slew rate or dV/dt of the filtered electrogram is so rapid in normal heart tissue that the difference between the peak and the nadir of the deflection is 5 milliseconds or less. On the other hand, diseased myocardium can conduct very slowly with fractionated electrograms, and this makes local events harder to identify. To acquire true local electrical activity, a bipolar electrogram with an interelectrode distance of less than 1 cm is preferable. However, in the setting of complex multicomponent bipolar electrograms, such as those with marked fractionation and prolonged duration seen in regions with complex conduction patterns, determination of local activation time becomes problematic. It is important to recognize, however, that clippers eliminate the ability to determine the amplitude and timing of the intrinsic deflection (local timing) of the signals being clipped. Intracardiac leads can be placed strategically at various locations within the cardiac chambers to record local events in the region of the lead. The recorded atrial electrogram is earlier in the P wave when the catheter is positioned close to the sinus node. Using a 5- to 10-mm bipolar recording, the His potential appears as a rapid biphasic spike, 15 to 25 milliseconds in duration, interposed between local atrial and ventricular electrograms. The use of a quadripolar catheter allows simultaneous recording of three bipolar pairs. The most proximal electrodes displaying the His potential should be chosen,and a large atrial electrogram should accompany the proximal His potential. Even if a large His potential is recorded in association with a small atrial electrogram, the catheter should be withdrawn to obtain a His potential associated with a larger atrial electrogram. Atrial pacing can be necessary to distinguish a true His potential from a multicomponent atrial electrogram. Not enough data, however, are available to define normal responses under these circumstances. For refractory periods, a speed of 150 to 200 mm/sec is adequate, but for detailed mapping, a speed of 200 to 400 mm/sec is required. Activation also propagates through the mid-atrial septum at the fossa ovalis and at the region of the central fibrous trigone at the apex of the triangle of Koch. Programmed Electrical Stimulation Stimulators Cardiac stimulation is carried out by delivering a pulse of electrical current through the electrode catheter from an external pacemaker (stimulator) to the cardiac surface. Such an electrical impulse depolarizes cardiac tissue near the pacing electrode, which then propagates through the heart. The paced impulses (stimuli) are introduced in predetermined patterns and at precise timed intervals using a programmable stimulator. Additionally, current stimulators have at least two different channels of stimulation (preferably four) and allow delivery of multiple extrastimuli (three or more) and synchronization of the pacing stimuli to selected electrograms during intrinsic or paced rhythms. Pacing threshold is defined as the lowest current required for consistent capture determined in late diastole. High current strength is generally used for determination of strength-interval curves to overcome drug-induced prolongation of refractoriness, assess the presence and mechanism of antiarrhythmic therapy, and overcome the effect of decreased tissue excitability.

True pain can occur at any time in the course of the evolution of the disease hair loss cure found 2015 generic dutas 0.5mg overnight delivery, may be felt almost anywhere in the upper limb hair loss cure 7th cheap 0.5mg dutas overnight delivery, ranges in severity from mild to excruciating hair loss in men wear discount generic dutas uk, or can be entirely absent hair loss diabetes order dutas 0.5mg without prescription. The system we use is designed so that it can be applied largely independently of the differing normal values of individual laboratories and shows a clear relationship with surgical prognosis hair loss hormone imbalance buy discount dutas 0.5mg online. When the diagnosis is unlikely on clinical grounds then the neurophysiologist should remember that false positive results on nerve conduction studies become commoner the more tests are performed (22) hair loss clinic generic 0.5 mg dutas otc, not concentrate too much on median nerve testing, and ensure that other neurological causes, which might explain the symptoms are tested for when possible. Instead testing should establish two things: How bad is the objective median nerve dysfunction This can range physiologically from no detectable impairment to no detectable function in the nerve. Although it has been argued that nerve conduction study reports should give no indication of the severity of disease (17), one of the main advantages of carrying out physiological measurements of this type is precisely that the degree of nerve dysfunction can be approached in a quantitative rather than qualitative manner. Studies of median sensory conduction between a median innervated digit and the wrist. A study of median motor conduction from wrist to a median innervated muscle, usually abductor pollicis brevis. Studies of enough other nerves to demonstrate that any local median nerve abnormality at the carpal tunnel is not simply part of a wider disorder. Testing such asymptomatic hands will often reveal nerve conduction evidence of mild median nerve impairment and provides useful baseline data for comparison when symptoms do develop in the second hand. The most extensively studied parameter is the cross sectional area of the median nerve just proximal to the carpal tunnel, either in absolute terms or in comparison to a more proximal section of the nerve. The exact reasons for such variation are not yet known, but probably include differences in the scanners themselves, the transducer frequencies, measurement methods, and operator variables. Among these findings are unusually proximal branching of the median nerve, persistent median arteries, intracarpal ganglion cysts, anomalous muscle bellies passing through the tunnel or invading it with wrist and finger movement, and median nerve tumours and malformations. These findings are analogous to the ability of nerve conduction studies to detect problems such as an underlying neuropathy and full assessment of a case of carpal tunnel syndrome should ideally include both modalities. Nerve conduction testing in these patients can be confusing, especially when no pre-treatment results are available, but can sometimes contribute to further clinical management. In the case of failed surgery for carpal tunnel syndrome the main decision to be made is whether to embark on more surgery. This is appropriate in two circumstances, firstly when the surgeon has directly injured a nerve during the operation, and secondly when the attempt to section the transverse carpal ligament has been unsuccessful. Partial division of the ligament is surprisingly common, accounting for about half of all unsatisfactory clinical outcomes in one large study (29). Both iatrogenic nerve injury and incomplete division of the ligament generally manifest as deterioration in nerve conduction study results compared with pre-operative tests. However full release of the ligament without any inadvertent injury, even when wholly clinically successful, is frequently not accompanied by return of either neurophysiological or imaging measurements of the median nerve to the normal range. The best known iatrogenic nerve injury during carpal tunnel decompression is to the recurrent motor branch of the median nerve leading to weakness and wasting of abductor pollicis brevis. Lacerations to the main median nerve trunk and to the palmar and digital branches of the median nerve are also documented (29). Patients with no recordable sensory or motor conduction in the median nerve, fixed sensory loss and marked thenar wasting may have little or no improvement even with correctly performed surgery though many will report some benefit, especially if they had troublesome pain and paraesthesiae before surgery (30). Post-operatively their nerve conduction studies may be improved, but seldom return to normal. This fibrous layer separates the triceps muscle mass of the upper arm from the biceps and brachialis compartment anteriorly on the medial side of the humerus. It is perforated by the ulnar nerve and thus forms a point at which the nerve is relatively fixed in place and potentially compressed. The condylar groove between the olecranon process and medial epicondyle of the humerus. The cubital tunnel-formed by the two heads of flexor carpi ulnaris and the aponeurosis, which joins them superficially and the medial ligaments of the elbow beneath. Ulnar neuropathy at the elbow Focal impairment of ulnar nerve function in the region of the elbow is the second commonest localized neuropathy, but is only 1/10th as common as carpal tunnel syndrome, is much more heterogeneous pathologically and clinically, and even less predictable in its clinical course and response to treatment. The incidence has been estimated at approximately 25 per 100,000 person years in Italy (31). Furthermore, the anatomical arrangement of the nerve at the elbow renders the ulnar nerve technically harder to test reliably using neurophysiological methods. In contrast to the general agreement about the exact site of damage to the median nerve in carpal tunnel syndrome, under the Very localized impairments of ulnar nerve conduction at these sites have been demonstrated using intra-operative nerve conduction studies, but the accuracy with which they can be identified using surface studies, even inching techniques, is uncertain (32) and ulnar nerve impairment in any given individual is not necessarily confined to only one of them. It is likely that the mechanical stresses on the nerve at these points are much more varied than the high tissue pressure which is found in the carpal tunnel, consisting of external pressure related to elbow position in daily activities, direct pressure from some of the structures listed above, and stretching of the nerve related to limb position. Nerve conduction studies may fail to demonstrate any abnormality at all in some patients with quite clear ulnar nerve signs and symptoms. These lesions produce a gradually worsening foot drop with sensory disturbance and sometimes pain and should be suspected in patients who develop a peroneal palsy in the absence of any history of a postural cause. They produce localized impairment of peroneal motor conduction in the region of the fibular head and popliteal fossa and are easily identified on ultrasound imaging They are very amenable to surgical treatment though it is essential to sever the connection with the tibiofibular joint, sacrificing the nerve branch, or else they recur. No systematic studies are available to help guide the interpretation of nerve conduction studies at the elbow after unsuccessful surgery. Peroneal neuropathy Acute or chronic compressive injury to the common peroneal nerve as it winds around the head of the fibula, resulting from prolonged kneeling or habitual sitting with one leg crossed over the other, is generally familiar as perhaps the third most commonly seen focal neuropathy, presenting as a foot drop with a variable sensory disturbance. It should be noted that a similar presentation can occur with a more proximal sciatic nerve lesion in which the peroneal nerve component of the sciatic nerve seems to be more vulnerable to injury in the region of the hip. This is a rare, but well documented event during hip replacement with an incidence of 0. At the knee however, this nerve provides a good illustration of how a strikingly unusual lesion can lead to a focal neuropathy. However, the weak point in the joint capsule of the tibiofibular joint from which these arise is the point at which the nerve branch from the peroneal nerve to the joint capsule enters it. As a result the cyst tracks up this nerve Tarsal Tunnel Syndrome-an example of a debatable syndrome the general success of the diagnosis of carpal tunnel syndrome as an explanation for median nerve impairment at the wrist leading to successful surgical treatment led logically to thoughts that a similar situation might be found in the foot and the term tarsal-tunnel syndrome was coined by two authors in 1962 (38,39). The anatomical analogue of the median nerve in the wrist at the ankle is the posterior tibial nerve as it passes behind and under the medial malleolus. As with the transverse carpal ligament at the wrist overlying the median nerve the posterior tibial nerve at this point does lie under a recognizable fibrous band, the laciniate ligament, also referred to as the internal angular ligament or the flexor retinaculum of the foot, which connects the medial malleolus to the calcaneum. Unlike the flexor retinaculum in the hand however, the laciniate ligament is not required structurally to resist the sort of forces applied to the flexor retinaculum of the hand by the long flexor tendons during wrist flexion and power grip. As a result it is a comparatively flimsy structure compared to the flexor retinaculum of the hand. The general principles of clinical assessment and testing set out in the first part of this chapter can be applied to suspected cases of tarsal tunnel syndrome, but the role of imaging is perhaps more important given the frequency with which anatomical explanations for a lesion are present. Conclusions Localized impairment of nerve function challenges the neurophysiologist to identify the site and severity of a lesion and the presence of any underlying or co-existing neuromuscular disorder. Aetiology can sometimes be inferred from the history and recognition of common clinical syndromes, but will often be clarified by imaging studies, especially with ultrasound, which can be performed at the same visit as the nerve conduction studies. The examiner should always adapt their approach to the clinical problem to meet the needs of the patient and any referring clinician in trying to make practical decisions on further management. Median nerve stiffness measurement by shear wave elastography: a potential sonographic method in the diagnosis of carpal tunnel syndrome. Comparison of second lumbrical and interosseus latencies with standard measures of median nerve function across the carpal tunnel: a prospective study of 450 hands. Reliability and validity of physical examination tests used to examine the upper extremity (letter). Neurophysiological classification of carpal tunnel syndrome assessment of 600 symptomatic hands. Evidence-based guideline: Neuromuscular ultrasound for diagnosis of carpal tunnel syndrome. The sensitivity and specificity of ultrasound for the diagnosis of carpal tunnel syndrome: a meta-analysis. Meta-analysis on the performance of sonography for the diagnosis of carpal tunnel syndrome. Ultrasonography for diagnosing carpal tunnel syndrome: a meta-analysis of diagnostic test accuracy. Revision surgery after carpal tunnel release: analysis of the pathology in 200 cases during a 2-year period. Management of extreme carpal tunnel syndrome: evidence from a long-term follow-up study. Peroneal and tibial intraneural ganglion cysts in the knee region: a technical note. Short segment incremental studies in the evaluation of ulnar neuropathy at the elbow. American Association of Electrodiagnostic Medicine, American Academy of Neurology, and American Academy of Physical Medicine and Rehabilitation. Ulnar neuropathy at the elbow: follow-up and prognostic factors determining outcome. Questions should be asked about the date of onset, rate of progression (in days, months, or years), onset in hands or feet, medication, family history, and presence of motor symptoms, sensory symptoms, asymmetry, pain, and autonomic symptoms. This information is helpful for choosing the appropriate electrophysiological protocol and for reassuring the patient that the rather unpleasant electrophysiological examination will be performed by a genuinely interested human being. For the latter reason, it is also essential to take the history and start the examination with the patient supine and covered by a blanket. The main purposes of the electrophysiological examination are to establish: stimulator perpendicular to the nerve until the largest response is obtained. At this site, the recording electrode is placed and the reference electrode 3cm more distally. Whether the polyneuropathy is related to demyelination of intact axons (demyelinating polyneuropathy), or to loss of axons without preceding demyelination (axonal polyneuropathy). It is, therefore, necessary to take account of limb temperature in order to avoid attributing abnormal variables to polyneuropathy whereas, in fact, they are due to decreased nerve temperature. Because nerves are buried in tissue, nerve temperature changes slowly over tens of minutes toward the desired value according to a decaying exponential function. Increase the stimulus current in steps of about 5 mA until a small response is obtained. Infrared heaters are unsuitable to raise limb temperature as warming by this method takes a very long time. Pathophysiology of single axons In normal myelinated axons, the action potential or impulse propagates because, at an active node, transient Na-channels open and Na-ions flow into the axon. This action current depolarizes the membrane, resulting in more Na-channel openings and further depolarization. The action current induces a current loop between the active node and the next node that has to be activated. At critically demyelinated internodes, driving current may just be sufficient for impulse propagation. Temperature increase may induce heat block because action current is reduced due to the shortened Na-channel open-time and faster fast K-channel opening. Prolonged duration or high frequency of firing of action potentials may induce rate-dependent block by several mechanisms of which hyperpolarization induced by increased activity of the electrogenic Na/ K- pump is the most important. Axonal degeneration may occur as a downstream effect of one of the mechanisms causing intra-axonal Na-accumulation (4). These include: increased Na-channel expression along a competely demyelinated internode and Na/K-pump dysfunction due to inflammation, ischaemia, or axonal transport deficits. Intra-axonal Na-accumulation induces reversed operation of the Na/Ca-exchanger in order to remove the excess Na-ions in exchange for Ca-ions, intra-axonal Ca-accumulation, and Camediated axonal degeneration. The rather simplified approach in clinical neurology is justified because it serves the practical purpose of establishing diagnosis. Pathological studies, however, may clearly show demyelination in clinically defined axonal neuropathies such as diabetic neuropathy, or show axonal degeneration in clinically defined demyelinating neuropathies. When this node is sufficiently depolarized, its Na-channels open and the outward driving current changes into the inward action current of the next action potential. The impulse at the first activated node is terminated because its Na-channels close after 1 ms, a process known as inactivation. Note that, when an ion-channel opens, it is the capacitative return current, which determines membrane potential change! Thus, Nachannel opening induces an inward Na-ion current along the Naconcentration gradient and an outward capacitative return current, which drops positive charges on the inside of the membrane and removes positive charges from its outside, thereby depolarizing the membrane. K-channel opening induces an outward K-ion current along the K-concentration gradient and an inward capacitative return current, which drops positive charges on the outside of the membrane and removes positive charges from its inside, thereby re- or hyperpolarizing the membrane. Leakage through the damaged myelin decreases driving current, resulting in more time being needed to depolarize a node and, thereby, slowing of internodal conduction time. Only after upregulation of internodal Na-channel expression will conduction be restored. The arrows refer to the direction of current through the channel if it is open under normal physiological conditions. Nat, transient Na-current, which sustains the impulse; Nap, persistent Na-current, which facilitates excitation; Ks, slow K-current which protects the axon against extreme depolarization; Kf, fast K-current, which avoids spreading of the impulse to the internode. Ih, hyperpolarization-activated cation current, which protects the axon against extreme hyperpolarization; 2K/3Na, Na/K-pump which maintains ionic concentration gradients. Chronic polyneuropathy Sensorimotor, symmetric, axonal Metabolic (diabetes, renal failure, hypothyroidism). Inherited childhood disorders (metachromatic leucodystrofia, adrenomyeloneuropathy, Refsum disease, Tangier disease, Krabbe leucodystrofia, Cockayne syndrome, cerebrotendinous xanthomatosis). This is because part of the nerve action potentials, evoked at the proximal site, will not pass the site where they are blocked, whereas the nerve action potentials, evoked at the distal site, will all reach the muscle.

Responses to single pulse electrical stimulation identify epileptogenesis in the human brain in vivo hair loss 6 months after hair transplant dutas 0.5mg with amex. Responsive cortical stimulation for the treatment of medically intractable partial epilepsy hair loss pills buy dutas 0.5mg fast delivery. Furlong hair loss 4 month old baby dutas 0.5 mg cheap, Elaine Foley hair loss zyprexa cheap dutas online mastercard, Caroline Witton hair loss quiz order dutas in united states online, and Stefano Seri Introduction For presurgical evaluation prior to lesionectomy hair loss in men 80s costumes buy dutas us, non- invasive neuroimaging has played an increasingly important role in the last decade, in planning procedures and evaluating associated risks. In patients with drug-resistant epilepsy, surgical resection of epileptogenic brain tissue affords an important prospect for seizure reduction or prevention, provided that the epileptogenic zone can be accurately defined and that its relationship to functionally important cortex is known. Neuroimaging techniques have aided in the non-invasive pre-surgical evaluation of these questions. This chapter attempts to summarize the key findings of these studies and the methodological developments that have improved clinical application. The calculation of the magnetic field is more straightforward than that of the electric field because of the symmetries and conductivity distribution of the human head. Once the spontaneous or evoked activity has been appropriately identified, the next vital element is to localize the sources of this activity with sufficient robustness to be of clinical value. However, there is now sufficient consensus and numbers of clinical trials to be able to summarize the key approaches. Source modelling All currents, both intracellular and extracellular, generate magnetic fields. Due to the near-spherical shape of the head, the resultant magnetic fields due to primary currents may be calculated without taking into account the conductivity layers of the head. The inverse solution of electromagnetic measurements is non-unique and mathematically ill-posed. Some of the most commonly used source analysis methods used clinically are discussed below. This is then optimally aligned using an iterative least-squares fitting algorithm. Including some facial features is essential with this procedure to provide a unique position for the spherical head geometry. Upon application, the relationship of the coils with respect to head anatomy is achieved using a 3D digitizer. It is typically computed using an iterative least- squares algorithm, which provides a goodness-of-fit measure to match the predicted solution with the actual data. Confidence volumes based on signal to noise estimates provide important measures to evaluate the robustness of localization (1,2). This approach is particularly effective for localizing evokedresponse activity in primary sensory areas and also in focal epilepsies. Nevertheless, correct identification of artefacts and abnormal transients will be an entirely familiar process to the trained clinical neurophysiologist. For mapping epileptiform activity, segments of the brain signal are used for source analysis, often without any signal averaging. This makes it possible to localize changes in spectral power or functional connectivity that can be used to make evoked, or resting state functional connectivity measures. Importantly, the signal amplitude of the spike above the ambient signal needs to be significant. There needs to be an evaluation as to whether the spike activity is best modelled with either a single equivalent dipole source or multiple equivalent sources, and the method requires an initial subjective evaluation about the number and putative location of these sources. Nevertheless, the technique is widely used and appears robust in the hands of skilled practitioners if the preconditions are met (3). With this method, the time-course of activity is examined for excess kurtosis and the spatial locations of voxels with high excess kurtosis are assumed to be sources of interictal spikes. The advantage of the technique is that the practitioner is presented with a series of automatically detected cortical locations with associated time series requiring no a-priori estimates of the number or putative location of spikes, and is independent of the spike amplitudes. Skilled practitioners are still required to exclude false positive kurtotic measures that may result from artefacts. The technique is particular valuable in this case since previous surgery distorts the visible gyral anatomy. Some of the problems of multiple dipole fitting, including the reliable estimation of the dipole location parameters, can be overcome by using a distributed source model that simultaneously models a large number of spatially fixed dipoles whose amplitudes are estimated from the data. The minimum norm estimate (5) is an example of such a distributed source model, and it allows the examination of the time course of activation at the source, which can be valuable in spike source estimations (6). Beamformer Another distributed source solution is the beamformer, which is based on the principal of spatial filters. The technique requires no a-priori assumptions relating to the number or notional position of the dipole sources. Panel B depicts the analysis pipeline employed to produce a source localization from the excess kurtosis defined data shown in Panel A. Other distributed source models have proven valuable in analysis of epileptiform data and the ability to explore the time course of spike propagation, and thus delineate the onset of epileptic activities has been reported (16). Functional connectivity Functional connectivity refers to coupled activity in anatomically distinct regions of the brain, such that if two areas are highly coupled in their activity over time, they are considered functionally connected. The study of brain networks in a relaxed awake state and in the absence of a specific task has gained increasing attention, as spontaneous neural activity has been found to be highly structured at a large scale. The underlying anatomical connectivity structure between areas of the brain has been identified as being a key to the observed functional network connectivity. Abnormally high functional connectivity across small distances could influence epileptic spike generation and increased connectivity has been hypothesized to be responsible for the propagation and generalization of epilepsy. Other studies report anatomical site-dependent variance in concordance, with 90% or greater concordance in the inter-hemispheric and frontal orbital region, approximately 75% in the superior frontal, central, and lateral temporal regions, but only approximately 25% in the mesial temporal lobe (53). Medvedovsky (23) using a movement compensation algorithm (18), was able to make lengthy ictal recordings in 34 patients. One significant challenge is to determine the extent of neighbouring tissue that should be included in the resection in addition to the lesion removal. This includes lesions located in deep anatomical structures, such as peri-insular cortex (92). Secondary bilateral synchrony A relatively common epilepsy localization problem in extratemporal epilepsy is that of secondary bilateral synchrony. A similar level of non-epileptic recordings have also been reported in other studies (102,103). In their repeat cohort, new localizing or complementary information was achieved in 58%. Functional mapping the ability to accurately define functionally critical cortical areas has significant consequences on the extent of resection to avoid potential damage to these areas, and may compromise the eventual outcome. Robust techniques for localizing sensory-motor cortex have been developed, while a number of language and memory paradigms continue to be refined. The motor cortex may also be mapped by quantifying the changes in beta rhythm associated with movement. Language cortex evaluation Surgery for temporal lobe epilepsy is commonly a left anterior temporal lobectomy, making localization of cortex subserving language function an imperative in these cases. Language cortex, typically the posterior language cortex, also needs to be precisely localized when a lesion is located in the posterior temporal lobe. Language processes are complex and include phonological, lexical, and also semantic processes. Verbal memory encoding and retrieval occurs concurrently in virtually any task, making it difficult to separate language processing from working memory. Sequential dipole fitting to both auditory and visual words appear to provide robust lateralization of language function (117). Other approaches that have been compared favourably with Wada include an auditory verb generation task (118), a silent reading task (119), and an auditory stimulus sequence comprised of two one-syllable spoken words presented in an oddball paradigm without subject response (120). Other techniques that have been evaluated include a verb-generation task assessed pre- and post-operatively (121). Sensory-motor cortex localization Precise localization of the motor cortex and somatosensory cortex (central sulcus) is commonly required for fronto-parietal lesions or for frontal lobe epilepsy. In presurgical studies, somatosensory mapping is usually confined to a few digits, toes and the lip. One problem with mapping motor-activated neural activity for clinical purposes is that, even with simple spontaneous repetitive finger movement, proprioceptive activation of sensory cortex localizes to a post-central gyrus. A second challenge is that motor cortex sources tend to be orientated primarily radially in relation to the detecting coils (101). In some patients, invasive recordings may not be viable or repeatable, due to previous surgery, limited cooperation, young age, or comorbidities. Routine application has been shown to yield good results, complementing other methods, such as intraoperative electrical stimulation or the Wada test in patients with epilepsy. In this epilepsy surgery candidate, a dual-state beamformer was used to characterize the pattern of beta power changes in right and left hemispheres. Magnetoencephalography-theory, instrumentation, and application to noninvasive studies of the working human brain. Application of magnetoencephalography in epilepsy patients with widespread spike or slow-wave activity. Dynamic imaging of coherent sources: Studying neural interactions in the human brain. Automated localization of magnetoencephalographic interictal spikes by adaptive spatial filtering. Spatially filtered magnetoencephalography compared with electrocorticography to identify intrinsically epileptogenic focal cortical dysplasia. Validation of head movement correction and spatiotemporal signal space separation in magnetoencephalography. Clinical evidence for the utility of movement compensation algorithm in magnetoencephalography: Successful localization during focal seizure. Sensitivity and specificity of seizure-onset zone estimation by ictal magnetoencephalography. High-frequency oscillations and other electrophysiological biomarkers of epilepsy: clinical studies. Resection of ictal high-frequency oscillations leads to favorable surgical outcome in pediatric epilepsy. Interictal high-frequency oscillations (80-500 Hz) are an indicator of seizure onset areas independent of spikes in the human epileptic brain. Clinical significance of ictal high frequency oscillations in medial temporal lobe epilepsy. Frequency and spatial characteristics of high-frequency neuromagnetic signals in childhood epilepsy. Noninvasive localization of epileptogenic zones with ictal high-frequency neuromagnetic signals. Measuring temporal, spectral and spatial changes in electrophysiological brain network connectivity. Local functional connectivity as a pre-surgical tool for seizure focus identification in non-lesion, focal epilepsy. Lopes da Silva (Eds) Electroencephalography, basic principles, clinical applications and related fields, 5th edn, pp. Dynamic statistical parametric mapping for analyzing ictal magnetoencephalographic spikes in patients with intractable frontal lobe epilepsy. Interictal and ictal magnetoencephalographic study in patients with medial frontal lobe epilepsy. The applications of time-frequency analyses to ictal magnetoencephalography in neocortical epilepsy. Propagation of epileptic spikes reconstructed from spatiotemporal magnetoencephalographic and electroencephalographic source analysis. Single-pulse electrical stimulation helps to identify epileptogenic cortex in children. Single pulse electrical stimulation for identification of structural abnormalities and prediction of seizure outcome after epilepsy surgery: a prospective study. Intrinsic epileptogenicity of focal cortical dysplasia as revealed by magnetoencephalography and electrocorticography. Electroclinical and magnetoencephalographic studies in epilepsy patients with polymicrogyria. Single and multiple clusters of magnetoencephalographic dipoles in neocortical epilepsy: significance in characterizing the epileptogenic zone. Interictal magnetoencephalography and the irritative zone in the electrocorticogram. Non-supervised spatio-temporal analysis of interictal magnetic spikes: comparison with intracerebral recordings. The correlation between ictal semiology and magnetoencephalographic localization in frontal lobe epilepsy. Interictal magnetoencephalographic findings related with surgical outcomes in lesional and nonlesional neocortical epilepsy.

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A side to side difference in H-reflex latency of more than 1ms is said to be significant hair loss underactive thyroid cheap dutas 0.5mg free shipping. The problem that arises is of knowing precisely where the root has been stimulated (81) hair loss cure july 2013 cheap dutas 0.5 mg free shipping. Whereas with stimulation over the cervical vertebral column hair loss cure how long generic dutas 0.5mg with mastercard, current is focused into intervertebral foramina to excite nerve roots at this location (82) hair loss in men 8 pack generic 0.5 mg dutas amex, over the lumbar area roots may be excited in their parallel course within the spinal canal hair loss 2 years after pregnancy buy 0.5 mg dutas free shipping. Nevertheless hair loss in men kidney buy 0.5mg dutas free shipping, there are reports of magnetic lumbar root stimulation having clinical utility in lumbar radiculopathy by showing slowing of conduction in the relevant motor roots (76). The use of dermatomal somatosensory evoked potentials in lumbosacral radiculopathy (41,71,83) has shown inconsistent results and is currently not regarded as useful. Lumbosacral plexopathy Lumbosacral plexus lesions are much less common than those of the brachial plexus and are most commonly due to tumours, trauma, or haematomas due to coagulopathies. Radiation plexopathy Radiotherapy can cause fibrotic change in the tissues around the brachial or lumbar plexus and can produce weakness and/or dysaesthsiae, sometimes years after the radiation therapy. Diabetic oculomotor mononeuropathy: involvement of pupillomotor fibres with slow resolution. Extensive mononeuritis multiplex as a solitary presentation of polyarteritis nodosa. Vasculitic multiplex mononeuritis: polyarteritis nodosa versus cryoglobulinemic vasculitis. Transcutaneous cervical root stimulation in the diagnosis of multifocal motor neuropathy with conduction block. Hereditary neuropathy with liability to pressure palsies: the same molecular defect can result in diverse clinical presentation. Clinical, electrophysiologic, and molecular correlations in 13 families with hereditary neuropathy with liability to pressure palsies and a chromosome 17p11. Clinical, electrophysiological, and molecular findings in early onset hereditary neuropathy with liability to pressure palsy. Dermatomal somatosensory evoked potentials in unilateral lumbosacral radiculopathy. The cutaneous silent period is preserved in cervical radiculopathy: significance for the diagnosis of cervical myelopathy. Diagnostic utility of F waves in cervical radiculopathy: electrophysiological and magnetic resonance imaging correlation. The study of diagnostic efficacy of nerve conduction study parameters in cervical radiculopathy. The usefulness of central motor conduction studies in the localization of cord involvement in cervical spondylytic myelopathy. Systematic correlation of transcranial magnetic stimulation and magnetic resonance imaging in cervical spondylotic myelopathy. Amyotrophic lateral sclerosis versus cervical spondylotic myelopathy: a study using transcranial magnetic stimulation with recordings from the trapezius and limb muscles. Traumatic brachial plexus injury: electrodiagnostic findings from 111 patients in a tertiary care hospital in India. Combined brachial root and plexus lesions-typical sequelae of motor-bike accidents. The terrible triad: anterior dislocation of the shoulder associated with rupture of the rotator cuff and injury to the brachial plexus. Neurophysiological prediction of outcome in obstetric lesions of the brachial plexus. The H-reflex as a tool in neurophysiology: its limitations and uses in understanding nervous system function. Comparison of magnetic coil stimulation and needle electrical stimulation in the diagnosis of lumbosacral radiculopathy. Measurement of the electric field induced into inhomogeneous volume conductors by magnetic coils: application to human spinal neurogeometry. Electrical stimulation over the human vertebral column: which neural elements are excited Utility of electrodiagnostic testing in evaluating patients with lumbosacral radiculopathy: an evidence-based review. Diagnostic value of history, physical examination and needle electromyography in diagnosing lumbosacral radiculopathy. Clinical findings and electrodiagnostic testing in 108 consecutive cases of lumbosacral radiculopathy due to herniated disc. Somatosensory evoked potentials from dermatomal stimulation as an indicator of L5 and S1 radiculopathy. Specificity of needle electromyography for lumbar radiculopathy and plexopathy in 55- to 79-year-old asymptomatic subjects. Interrater reliability of needle electromyographic findings in lumbar radiculopathy. Neurophysiological tests, however, are not a substitute for clinical assessment and must always be designed and interpreted in relation to the clinical syndrome. Secondly, it may be helpful in staging the disorder and, thirdly, it can help in establishing the prognosis. Reinnervated muscle fibres assume the same histological characteristics as those of the reinnervating motor units. Newlyformed end-plates have immature acetyl choline receptor subunits, and a lower safety factor for neuromuscular transmission (6). A single muscle fibre action potential is used as the triggering source for studies of firing pattern, as well as the physical aspects of volume conduction. Changes in amplitude and area are probably more sensitive as an index of neurogenic change than increased duration. An increased number of satellite potentials are also often observed in early affected muscles (10). Active denervation Fibrillation and positive sharp-waves at rest, which are considered a cardinal sign of denervation (18), are non-specific findings that can be recorded in myopathies, as well as in any neurogenic disorder. They represent action potentials generated by individual muscle fibres that have lost their nerve supply, either by axonal damage or by direct muscle fibre damage. Both fibrillation (fib) and positive sharp-waves (p-sw) appear to be generated from a biphasic intracellular action potential with a long hyperpolarization phase (19). The presence of abundant and diffuse fibs-sw is considered a poor prognostic sign (3). This number represents a correlate of fibre grouping observed in histological samples (6). The neuromuscular jitter gives information about the stability of neuromuscular transmission (6). Mills (39) suggests that 90s of observation is required in each tested concentric needle insertion. Its origin seems to be ephaptic transmission through an excitatory loop between adjacent muscle fibres (41). Such discharges, characteristic of membrane disturbance, may also be observed in patients with other long-lasting neurogenic disorders, such as radiculopathies and radiation plexopathy. They can arise in abnormal, reinnervated, surviving motor units, or from a generator localized in the distal axonal branches (35,36). This issue is particularly critical in cranial-innervated muscles since fibs-sw is not so frequently observed in these muscles (21). However, it is very difficult to relax the tongue, in order to show fib-sw, and performing many needle insertions of the tongue is too invasive in clinical practice. However, the tongue is probably a more sensitive muscle to study for showing fibs-sw than the masseter, temporalis, frontalis, and mentalis muscles (42,43). Histological evidence of selective loss of large myelinated nerve fibres has been noted (63), but in other studies no preferential involvement of fast conducting fibres was found (64). Both the maximal and minimal motor conduction velocities are slowed (64), suggesting that faster and slower conducting motor fibres are similarly susceptible. This finding is consistent with the histological finding of involvement of somatic extrafusal and intrafusal (gamma) motor fibres in the disease (65). In routine conduction studies only the fastest-conducting, large myelinated fibres are evaluated. The collision technique allows assessment of both the fast and slow conducting motor fibres in a motor nerve (66). In particular the first dorsal interosseous is sensitive (21,48), easily investigated in all patients, and usually more severely affected than the abductor digiti minimi. Abdominal muscles, internal intercostal muscles activated during expiration, and diaphragm activated during inspiration, are other useful muscles for testing. Denervation of the respiratory muscles indicates impending respiratory failure (54). Involvement of the respiratory muscles and diaphragm is associated with denervation of paraspinal muscles (55), but diaphragmatic involvement cannot be predicted from involvement of limb muscles in the same myotome (56). In our experience (21) patients with lower-limb onset always show fibs-sw in lower limb muscles, and the same is almost always true for patients in whom the weakness commences in upper limbs, when fibs-sw are easily found in first dorsal interosseous muscle. It is important to understand that when one limb is affected, the next to be involved is often the homologous contralateral muscle, indicating the characteristic mode of spread of disease to contiguous motor neuronal cell columns within the cord (57). Although it is often stated that F-wave frequency is also increased, this assertion is poorly documented (68,69). F-waves show increased latency and dispersion, and there may be an increased frequency of repeater F-waves (69). The H reflex (Hoffmann reflex) is a monosynaptic response, which assesses the integrity of both motor and sensory nerve fibres, and the nerve excitability at the spinal level. However, other changes may be observed, such as an increased H/M ratio, diminished inhibition of the H-reflex by simultaneous vibratory stimulation of the soleus muscle or its tendon, and lesser reduction of the amplitude of the H-reflex in a paired-stimulation paradigm (71). Probably, this abnormal decrement results from disturbed electrical conduction through immature nerve terminals and neuromuscular junctions (74). Nevertheless it is a useful technique, readily mastered, and can detect abnormal spontaneous activity in the diaphragm as well as abnormalities of motor unit potentials recorded during inspiration (54). Percutaneous electrical stimulation of the phrenic nerve in the neck is simple and non-invasive (79,80). These electrophysiological studies should be considered in conjunction with functional pulmonary tests. Sensory conduction studies in amyotrophic lateral sclerosis Sensory potentials should always be studied to confirm that the disease process does not involve sensory neurons. Focal paranodal demyelination leads to dissipation of the action potential as a result of decreased impedance in the pathological region, so that depolarization of the next node fails to reach threshold, and conduction block occurs. Focal demyelination in motor nerves can be difficult to demonstrate, since it may occur proximal to the most proximal stimulation site, or more distal than the distal stimulation point, and may therefore resemble axonal loss. Root stimulation can be performed using high-voltage electrical stimulation, needle stimulation, or magnetic stimulation over the spine. However, the first two are poorly tolerated, and the stimulation obtained by the last method is not always maximal. In multifocal motor neuropathy with conduction block (59,60) only the motor nerve fibres are affected. In motor and sensory demyelinating neuropathy with conduction block (58) both the motor and sensory fibres are affected, although with motor predominance. Pure motor neuropathies have been described in patients with monoclonal gammopathy (108), a rare disease. Ideally, conduction block should be identified by stimulation over short nerve segments. Although such carefully defined criteria are useful, when conduction block is clinically relevant it is almost always very marked. It is important to establish an early diagnosis of focal demyelination, because patients with very wasted muscles are less likely to benefit from treatment with intravenous immunoglobulin (110). Reports of several patients diagnosed as multifocal motor neuropathy with conduction block who have been found at autopsy to have loss of anterior horn cells and Bunina bodies in motor neurons has increased the difficulties of diagnosis and understanding in this field (111). Nevertheless, these minor changes are not proportional to the degree of involvement of motor nerves (4), and when these studies are abnormal, another diagnosis should be suspected. More refined tests may discern some changes, as described using the near-nerve stimulation technique (87), measuring resistance to ischaemia (88), or testing quantitatively the threshold to vibration (89). Morphometry of the dorsal root ganglia showed some changes in sensory neurons (90) and loss of axons has been reported in the sural nerve (63), which may explain the abnormalities observed in some neurophysiological investigations. Threshold tracking is a complex technique of undetermined diagnostic utility although it may be useful in detecting axonal or neural hyperexcitability. Transcranial corticomotor stimulation studies There is evidence for increased excitability due to reduced inhibition in the motor cortex. In these circumstances the clinical neurophysiologist should consider the clinical picture before reaching any conclusion. Neuro-imaging is generally Differential diagnosis Demyelinating neuropathies Focal demyelination with partial conduction block causes weakness in demyelinating motor neuropathies. The differential diagnosis between post-polio and old polio with no progression, based on neurophysiological grounds is virtually impossible, since fibs-sw and increased jitter are common in residual polio, not indicating progressive disease (113).