Terazosin

John M. Murkin, MD, FRCPC

• Professor of Anesthesiology (Senate)
• Director of Cardiac Anesthesiology Research
• Schulich School of Medicine
• University of Western Ontario
• London, Ontario, Canada

If abnormalities are found in these muscles heart attack 25 generic 2 mg terazosin overnight delivery, a more extensive evaluation should be performed to sort out whether the changes are due to a proximal tibial neuropathy prehypertension risk factors cheap terazosin 5 mg buy on line, sciatic neuropathy enrique iglesias heart attack terazosin 2 mg, lumbosacral plexopathy blood pressure 40 year old woman purchase discount terazosin, radiculopathy hypertension age 70 generic 1 mg terazosin with amex, or polyneuropathy. Third, it may be theoretically hazardous to puncture the skin of the foot in a patient who is insensate and/ or has vascular insufficiency in the lower extremities. Distally in the tarsal tunnel, the nerve divides into the larger medial plantar and smaller lateral plantar nerves. To visualize the tibial nerve at the ankle, the patient is asked to lie supine on the bed with their legs slightly externally rotated. The probe is placed with one end over the medial malleolus and the other distally over the calcaneus. The large tendon of the tibialis posterior lies adjacent to the medial malleolus superiorly, with the smaller tendon of the flexor digitorum longus below. The tibial nerve is usually quite hyperechoic and easily visualized at the tarsal tunnel. As the nerve is followed distally toward the sole, it can commonly be seen dividing into the medial and lateral plantar nerves. Note the common pattern of the posterior tibial artery flanked by two veins adjacent to the tibial nerve. Bottom, Same images with the tibial nerve in yellow, ganglion cyst in green, and posterior acoustic enhancement designated by the red arrows. Note the large anechoic ganglion cyst located just above the tibial nerve, presumably exerting pressure on the distal tibial distal nerve. Ultrasound is very helpful in assessing for structural causes of tibial nerve entrapment at the tarsal tunnel. When inspecting the tibial nerve, one assesses the cross-sectional area, echogenicity, and fascicular structure, similar to other entrapment neuropathies. Lastly, if a patient has foot pain, especially with a "burning" feeling in the sole, the plantar fascia should be assessed. The probe is put in long axis with one end over the medial calcaneus and the other end in the mid-sole. The central fascia of the sole can then be followed both in long and short axis throughout the sole to the level of the metatarsal heads. In long axis, there is a large venous structure immediately adjacent to the enlarged tibial nerve. Looking at the vein in long axis, note the area on the far left-this is the normal size of the vein. A single enlarged vein is known as a varix, which rarely can result in compression of the nearby tibial nerve. Although this outpouching is enlarged, these outpouchings are normal areas where the valves are located within the vein. Bottom, Same images with the plantar fascia in purple and the medial calcaneus in green. The optimal location to assess for plantar fasciitis is where it inserts onto the medial calcaneus (white double-arrow). Four months previously, she sustained a nondisplaced fracture of the right ankle and wore a cast for 6 weeks. Sensation was intact over the outside of the lateral foot and the dorsum of the foot. Hypesthesia to pinprick and temperature was present over the sole of the right foot. The deep tendon reflexes, including the ankle reflexes, were present and symmetric. Persistent pain following trauma and an ankle fracture could very well be of local orthopedic origin. There is mild atrophy of the intrinsic foot muscles on the right, although with the history of recent casting, this finding could be due to disuse alone. The sensory examination shows normal sensation over the lateral foot and the dorsum of the foot, but pinprick and temperature sensation are decreased over the sole of the right foot. This pattern of abnormal sensation over the sole of the foot with complete sparing of the lateral foot and dorsum of the foot would be unusual for a typical polyneuropathy, in which all the distal fibers are affected equally. Numbness over the sole may be seen in disorders other than polyneuropathy, including proximal tibial neuropathy, sciatic neuropathy, lumbosacral plexopathy, or lesions of the S1­S2 nerve roots. For example, a lesion of the S1 nerve root, lumbosacral plexus, sciatic nerve, or more proximal tibial nerve may well result in an abnormal ankle reflex on the symptomatic side. When reviewing the nerve conduction studies, particular attention must be paid to whether the results correlate with the clinical examination. Peroneal motor studies are performed next on the symptomatic side; they are normal. After the motor studies are completed, the sensory studies are performed, including the sural and then the superficial peroneal sensory responses on the right side. The normal sural sensory response correlates with the normal sensation over the lateral foot, and the normal superficial peroneal sensory response likewise correlates well with the normal sensation over the dorsum of the foot. As for the plantar responses, when the medial and lateral plantar mixed nerves are recorded, only small-amplitude responses are obtained from the right side. This finding alone would not necessarily be considered abnormal, because plantar mixed and sensory responses often are very small or difficult to obtain in normal subjects. When these responses are compared with the asymptomatic contralateral side, however, the amplitudes are clearly and significantly asymmetric (>50% difference from side to side, comparing right to left). In addition, the latencies are somewhat prolonged on the right side compared with the left. The degree of prolongation is not in the unequivocally demyelinating range and may be consistent with axonal loss and dropout of the fastest-conducting fibers. When the nerve conduction studies are completed, there is strong evidence for a lesion affecting the distal tibial nerve and involving the medial and lateral plantar nerves. Polyneuropathy seems less likely, given the intact and robust sural and superficial peroneal sensory Chapter 27 · Tarsal Tunnel Syndrome 477 responses and the asymmetry of the plantar mixed nerve studies from side to side. However, the reduced amplitude of the medial and lateral plantar mixed nerve responses and the borderline prolonged latencies are well within the range that would indicate axonal loss. However, the fact that the sural sensory response is normal, which is derived proximally from the tibial and peroneal nerves in the popliteal fossa, argues against a proximal lesion of the tibial nerve. Normal subjects without any complaints may have mild active denervation or reinnervation (or both) in the intrinsic foot muscles. Next, two tibial-innervated muscles that arise above the tarsal tunnel are sampled (the medial gastrocnemius and the tibialis posterior), and both are entirely normal. The clinical findings of intact sensation over the lateral and dorsal foot also argue strongly against a polyneuropathy, sciatic neuropathy, or lumbosacral plexopathy. These findings are later substantiated on the nerve conduction studies, which show normal sural and superficial peroneal sensory responses. Note that the asymmetric abnormalities in the mixed nerve responses seen in this case would not be expected in a sacral radiculopathy, because sensory potentials (which make up the majority of mixed nerve potentials) are spared in lesions proximal to the dorsal root ganglion. Therefore, although the electrophysiology fails to definitively localize the lesion, the weight of the evidence favors a lesion of the distal tibial nerve at the ankle (medial and lateral plantar nerves), especially considering the site of the trauma and the site of the persistent pain. Electrophysiological improvement in tarsal tunnel syndrome following decompression surgery. Usefulness of electrodiagnostic techniques in the evaluation of suspected tarsal tunnel syndrome: an evidence-based review. The electrophysiologic abnormalities are limited to the distal tibial nerve, that is, the medial and lateral plantar nerves. The facial nerve can be directly stimulated and recorded using standard nerve conduction techniques. As in other neuromuscular disorders, the electrophysiologic evaluation of facial and trigeminal neuropathies is used to confirm localization of the lesion, assess the underlying pathophysiology and severity of the lesion, and offer a prognosis. In fact, assessment of severity and prognosis are often the key issues addressed by the electromyographer in the most common cranial neuropathy of all, idiopathic facial palsy. The facial motor root supplies the muscles of facial expression and arises from the facial motor nucleus located in the ventral lateral tegmentum of the lower pons. The nervus intermedius carries taste, sensory, and parasympathetic fibers and arises from the solitary nucleus/tract (medulla), trigeminal sensory nuclei (medulla-pons), and superior salivatory nucleus (pons), respectively. The facial nerve, including the motor root and nervus intermedius, emerges from the brainstem at the cerebellopontine angle and enters the internal auditory meatus, next passing through the geniculate ganglion before traversing the facial canal. First, parasympathetic fibers are given off to the greater and lesser petrosal nerves, bound for the pterygopalatine and otic ganglia. A small motor branch arises next, to innervate the stapedius muscle in the inner ear. The chorda tympani then arises to carry taste fibers to the anterior two-thirds of the tongue and parasympathetic fibers to the submandibular and sublingual salivary glands. The facial nerve exits the skull at the stylomastoid foramen before coursing through the parotid gland. After the stylomastoid foramen, the nerve supplies the stylohyoid and the posterior belly of the digastric muscles, then gives off a cutaneous posterior auricular branch before dividing into its five major peripheral branches: temporal (a. Trigeminal Nerve the trigeminal nerve, cranial nerve V, carries sensory fibers to the face and motor fibers to the muscles of mastication. It arises from several different nuclei in the brainstem, including one motor nucleus (mid-upper pons) and three separate sensory nuclei. The sensory nuclei include the main sensory nucleus (mid-upper pons), which mediates light touch; the nucleus of the spinal tract of V (pons to upper cervical cord), which mediates pain and temperature; and the mesencephalic nucleus of V (lower midbrain), which mediates proprioception from facial muscles. The facial nerve is formed by the merging of the facial motor root and the adjacent nervus intermedius. Within the bony facial canal, several branches arise from and leave the main facial nerve. Parasympathetic fibers are given off to the greater and lesser petrosal nerves, bound for the pterygopalatine and otic ganglia. A small motor branch arises next to innervate the stapedius muscle in the inner ear. The blue arrow indicates where fibers from the lingual nerve, a branch of V3, join the chorda tympani fibers. After exiting the stylomastoid foramen, the facial nerve bifurcates into five major peripheral branches: temporal, zygomatic, buccal, mandibular, and cervical to supply the muscles of facial expression. Exiting from the lateral mid-pons, the trigeminal nerve divides into three major peripheral nerves-ophthalmic (V1), maxillary (V2), and mandibular (V3)-which arise from the trigeminal ganglion, located just outside the brainstem on the petrous bone in the middle cranial fossa. The three branches of the trigeminal nerve-ophthalmic nerve (V1), maxillary nerve (V2), and mandibular nerve (V3)-supply sensation to the face and anterior scalp. Whereas the trigeminal ganglion contains cell bodies of the sensory fibers from both the main sensory nucleus and the nucleus of the spinal tract of V, the cell bodies of proprioceptive sensory fibers from muscle spindles of trigeminal motor fibers are contained within the mesencephalic nucleus of V in the midbrain. The three major peripheral nerve divisions of the trigeminal nerve are the ophthalmic (V 1), maxillary (V2), and mandibular (V3) nerves. Each nerve exits the skull through a distinct opening: (1) the ophthalmic nerve through the superior orbital fissure, (2) the maxillary nerve through the foramen rotundum, and (3) the mandibular nerve through the foramen ovale. Each of the three major nerve branches contains sensory fibers, whereas motor fibers are carried solely in the mandibular nerve branches that supply innervation to the muscles of mastication (masseter, temporalis, medial, and lateral pterygoid muscles) and to the anterior belly of the digastric muscle, the mylohyoid, tensor veli palatini, and tensor tympani muscles. Unilateral facial nerve dysfunction can also be seen in association with several disorders, most commonly in the setting of diabetes. In addition, facial palsy occurs with herpes zoster involving the geniculate ganglion (Ramsay Hunt syndrome), lymphoma, leprosy, cerebellopontine angle tumors such as acoustic neuroma, multiple sclerosis, stroke, and a host of other disorders (Box 28. Bilateral facial weakness is less common; it may be seen in Guillain- Barré syndrome, Lyme disease, sarcoid, Melkersson-Rosenthal syndrome, tuberculous meningitis, and leptomeningeal lymphomatosis/carcinomatosis. Bifacial weakness also is noted in some neuromuscular junction disorders and in various muscular dystrophies. Either type of aberrant reinnervation can result in synkinesis of facial movements. For example, closing the eye (orbicularis oculi) may be accompanied by movement of the lips (orbicularis oris). Clinically, these reinnervation abnormalities may vary from being very subtle to very severe. In the most extreme case, synkinesis may lead to massive contractions on one side of the face. As most people blink spontaneously every few seconds, synkinesis involving the orbicularis oculi and other facial muscles can clinically appear very similar to hemifacial spasm (see later), although the etiology is quite different. Aberrant reinnervation may also occur between the motor axons of the facial nerve and the parasympathetic axons. Thus, parasympathetic axons may innervate motor endplates, and, conversely, motor axons may innervate the parasympathetic endplates. This may result in lacrimation, salivation, and/or hemifacial sweating when the facial muscles are activated. One can imagine the embarrassing situation wherein tears rather than saliva are produced while eating. The clinical presentation of facial nerve palsy depends on the location, pathophysiology, and severity of the lesion. A central lesion (proximal to the facial nerve nuclei) causes contralateral weakness primarily of the lower facial musculature, with relative sparing of the orbicularis oculi and frontalis muscles, which are bilaterally innervated. Furthermore, with central lesions, there may be facial movement during laughing or crying because the pathways that mediate responses to emotional stimuli are different from those that mediate voluntary facial movement. Peripheral lesions (at or distal to the facial nerve nuclei) cause ipsilateral facial paralysis that affects both the upper and lower facial musculature, resulting in an inability to wrinkle the forehead, close the eye, or smile. In addition, there may be dysfunction or absent taste sensation over the anterior two-thirds of the tongue, depending on which branches are involved as the nerve courses through the facial canal. The etiology is thought to be inflammation of the facial nerve, which causes swelling and compression of the nerve in the facial canal. In most patients, the prognosis is excellent, with full recovery of function over several weeks to months.

Diseases

• Anterior horn disease
• Tosti Misciali Barbareschi syndrome
• Pfeiffer Palm Teller syndrome
• Selective mutism
• Landau Kleffner syndrome
• Camptodactyly overgrowth unusual facies
• Rapunzel syndrome
• Hypercalcemia, familial benign
• Generalized seizure
• Leukemia, Myeloid

The fibers that eventually form the peroneal division of the sciatic nerve lie posteriorly blood pressure 9664 purchase genuine terazosin line, closest to the bone blood pressure app for iphone purchase genuine terazosin on-line, and are more vulnerable to compression than the tibial division fibers wide pulse pressure young generic terazosin 5 mg buy online. Accordingly heart attack 8 trailer 5 mg terazosin buy mastercard, peroneal fibers are often most affected pulse pressure below 40 order terazosin 1 mg online, with some women presenting with a postpartum foot drop, not infrequently misdiagnosed as peroneal palsy at the fibular neck. In addition to peroneal weakness, examination often shows mild weakness of knee flexion (hamstrings) and hip abduction, extension, and internal rotation (glutei, tensor fascia latae), demonstrating that the lesion is clearly beyond the peroneal territory. Sensory disturbance is most marked over the dorsum of the foot and lateral calf but may be patchy and involve the sole of the foot, posterior calf, and thigh. Several factors predispose to this injury, including a first pregnancy, a large fetal head with a small maternal pelvis (cephalopelvic disproportion), a small mother (less than 5 feet in height), and a prolonged or difficult labor. Women who have experienced a prior episode are predisposed to this complication with additional pregnancies. Although rare patients may be left with permanent weakness, the prognosis is excellent in most cases. The presumed mechanism of injury involves compression that leads to ischemia and mechanical deformation of nerve fibers, which in turn lead to demyelination and, if severe enough, axonal loss. In the first stage, relatively rapid improvement occurs over days to weeks from remyelination of demyelinated fibers. This is followed by relative stabilization and a much slower recovery over many months to years from axonal regrowth and reinnervation. Diabetic Amyotrophy Painful lumbosacral plexopathy may occur in patients with diabetes mellitus. On nerve pathology, the underlying cause appears to be a microscopic vasculitis leading to nerve ischemia. They typically present with severe, deep boring Chapter 35 · Lumbosacral Plexopathy 629 pain in the pelvis or proximal thigh, which may last weeks (average is approximately 6 weeks). As the pain slowly abates, it becomes apparent that the patient also has significant weakness that is out of proportion to the pain. Diabetic amyotrophy commonly affects the femoral and obturator nerves, with prominent wasting of the anterior and medial thigh musculature. Despite the prominent pain, atrophy, and weakness, there may be very little sensory loss in the L2­L4 distribution. It is not unusual for patients who develop diabetic amyotrophy to have a coexistent diabetic polyneuropathy; accordingly, such patients will have some sensory disturbance and loss of reflexes in the distal legs as well. In others, the same process may affect the contralateral side within the first few weeks or months of initial presentation. Recovery often is good but usually quite prolonged, ranging from many months to 1­2 years. This entrapment is more common in patients who are obese; who wear tight underwear, pants, or belts; or who have diabetes. Although the vast majority of cases are due to an entrapment at the inguinal ligament, rare cases have resulted from trauma and others from tumors and other mass lesions compressing the nerve. Beyond the obvious function of localizing the lesion, electrophysiologic studies are useful in assessing severity and chronicity, as well as in Radiation Plexopathy Similar to radiation-induced brachial plexopathy, lumbosacral plexopathy can also occur from radiation damage, usually as a result of radiation administered years previously for treatment of a tumor. Clinically, myokymia is recognized as rippling, undulating, or wormlike movement of muscles. Notably, myokymia is not seen in direct tumor invasion of the plexus and is an important marker of radiation-induced damage. The clinical syndrome, known as meralgia paresthetica, results in a painful, burning, numb patch of skin over the anterior and lateral thigh. Because there is no muscular innervation from this nerve, there is no associated muscle atrophy, weakness, or loss of reflexes. Tibial motor study, recording the abductor hallucis brevis, stimulating the medial ankle and popliteal fossa; bilateral studies 2. Peroneal motor study, recording the extensor digitorum brevis, stimulating the ankle, below the fibular neck and lateral popliteal fossa; bilateral studies. In patients with an isolated foot drop and clinical findings limited to the distribution of the peroneal nerve, recording the tibialis anterior, stimulating below fibular neck and lateral popliteal fossa, should be performed to increase the yield of demonstrating conduction block or focal slowing across the fibular neck 3. Sural sensory study, stimulating posterior calf, recording posterior ankle; bilateral studies 4. H reflex; bilateral studies Additional studies for suspected lumbar plexopathy or lateral femoral cutaneous neuropathy: 1. Saphenous sensory study, stimulating medial calf, recording medial ankle; bilateral studies 2. Femoral motor study, stimulating the femoral nerve at the inguinal ligament, recording the rectus femoris; bilateral studies 3. Lateral cutaneous nerve of the thigh sensory study, stimulating just medial to the anterior superior iliac spine, recording over anterior thigh; bilateral studies Special consideration: If symptoms are bilateral, consider studying an upper extremity to exclude polyneuropathy. Nerve Conduction Studies the nerve conduction evaluation of lumbosacral plexopathy is outlined in Box 35. Careful attention must be paid to the peroneal motor study, with the electromyographer looking for evidence of peroneal palsy at the fibular neck (either focal slowing or conduction block) in patients with foot drop. In lumbar plexopathies, femoral motor studies can also be performed bilaterally to assess the amount of axonal loss. Likewise, if there has been loss of the fastest conducting axons, there may also be mild prolongation of the distal motor latencies and some slight slowing of conduction velocity. If only the upper lumbar plexus is involved, routine peroneal and tibial motor studies may be completely normal. In a lower lumbosacral plexopathy, the peroneal and tibial F responses may be more prolonged on the symptomatic side than on the asymptomatic side. Likewise, the H reflex may be prolonged or more difficult to elicit on the involved side. Of course, the finding of prolonged or absent F and H responses on one side cannot be used to differentiate among a sciatic neuropathy, lumbosacral plexopathy, or radiculopathy, but a proximal lesion is implied if the distal conduction studies are normal. Both superficial peroneal and sural sensory studies should be performed in a suspected lower lumbosacral plexopathy, and saphenous studies should be included for a suspected upper lumbar plexopathy. These studies, however, often are difficult to perform using surface electrodes, especially in obese patients. If a response cannot be obtained by moving the stimulator, then one should also try to move the recording electrodes parallel to the initial placement. Because this response is difficult to obtain in many normal individuals, it ideally should be compared with the contralateral, asymptomatic side, in cases where only one side is affected. Any side-to-side difference in amplitude of more than 60% (comparing the higher with the lower side) is considered abnormal. In a study using the technique described earlier, Boon and colleagues found an absent response on one or both sides in 8% of normal individuals. These data underscore the limitation of this study when responses are absent or very low. If the patient has unilateral symptoms, it is often best to start with the uninvolved, asymptomatic side. Clearly, in obese patients (note, obesity is a risk factor for this condition), the study is even more technically difficult. If no response can be elicited on the asymptomatic side, there is little use in trying to obtain the potential on the involved side. Although abnormal sensory conduction studies can define the lesion as at or distal to the dorsal root ganglion, they usually cannot separate a mononeuropathy from a plexopathy. In mononeuropathy, abnormalities are limited to one nerve, whereas in plexopathy, more than one nerve is involved. The gluteal muscles are especially useful in separating a sciatic neuropathy from a lower lumbosacral plexopathy, as any abnormalities in the gluteal muscles place the lesion at or proximal to the plexus, thereby excluding an isolated sciatic neuropathy. Likewise, in the differentiation of femoral neuropathy from upper lumbar plexopathy, abnormalities in the thigh adductors, which are innervated by the obturator nerve, place the lesion at or proximal to the lumbar plexus, thereby excluding an isolated lesion of the femoral nerve. Lastly, the evaluation of the paraspinal muscles is extremely important in separating lesions of the plexus from the nerve roots. However, the absence of abnormalities in the paraspinal muscles cannot definitively exclude a lesion of the nerve roots. Because this is actually a lumbosacral radiculoplexopathy, it is not unusual for the paraspinal muscles to be involved. The classic electrophysiologic picture of an upper lumbar plexopathy is that of normal tibial and peroneal motor conduction studies along with normal F responses and H reflexes. Both the sural and superficial peroneal sensory nerves are normal, but the saphenous sensory response is reduced or absent on the involved side. If there has been axonal loss, the femoral motor amplitude will be lower on the affected side. In some patients, peronealand superior gluteal-innervated muscles that have partial L4 innervation. Likewise, the tibial and peroneal F responses often are prolonged or absent on the symptomatic size, with similar findings for the H reflex. Both the sural and superficial peroneal sensory nerves are reduced in amplitude or absent, with normal potentials on the contralateral asymptomatic side. In superficial muscles, myokymia can be recognized clinically by an undulating, wormlike movement of the muscle. However, in suspected lateral cutaneous neuropathy of the thigh, it is important to exclude a lumbar plexopathy and especially an L2 radiculopathy. In this regard, the iliacus, thigh adductors, and less so the quadriceps are important muscles to check. It is well recognized that the paraspinal muscles are normal in many cases of radiculopathy (approximately 50% in many series). This may be due to fascicular sparing of some fibers, sampling error, or difficulty examining the paraspinal muscles due to poor relaxation. In addition, reinnervation, like denervation, occurs first in the most proximal muscles. If the Lesion Is Acute, the Study May Be Normal Patients with painful lumbosacral plexopathy may be referred early in the course of their illness for an evaluation. During the first week, however, nerve conduction studies may remain completely normal, as there has not been enough time for wallerian degeneration to have occurred. Bilateral Lumbosacral Plexopathy Is Difficult to Differentiate From Polyneuropathy Although most lumbosacral plexopathies are unilateral, some may be bilateral, including those caused by tumor, radiation, and diabetes. In such cases, it may be very difficult to differentiate a lumbosacral plexopathy from a polyneuropathy. However, ultrasound can visualize some of the major nerves derived from the lumbosacral plexus. Ultrasound of the femoral nerve is discussed in Chapter 26, and the sciatic nerve is discussed in Chapter 36. As the nerve conduction study is technically challenging, especially in obese patients, it is frequently difficult to know how to interpret an absent response, especially if the response is absent bilaterally. In these cases, ultrasound may be particularly useful in confirming an abnormality. As bone is hyperechoic with prominent posterior acoustic shadowing, it is easy to identify. When the probe is placed in short axis over the anterior ilium, bone is easily identified. Once it is identified, it can be followed distally into the proximal thigh, where is becomes subcutaneous. Once the nerve is identified, it can be followed distally into the proximal thigh, where it becomes subcutaneous. When the nerve is entrapped, it becomes enlarged and hypoechoic and is much easier to identify. Indeed, if one has difficulty finding the nerve, it most often means that the nerve is normal. However, the results are only slightly better than the standard study using surface landmarks. Summary the history is that of a young girl with hemophilia who presented with a 2-week history of sudden-onset, severe right groin pain that increased over several hours and persisted. The neurologic examination is notable for an absent right knee jerk and hypesthesia over the right medial calf. The right hip is flexed and externally rotated, and strength cannot be reliably assessed because of the pain. Femoral motor studies and contralateral left tibial and peroneal motor studies were not performed because the patient was in severe pain, and the test was curtailed. It was more important to perform bilateral sensory conduction studies to determine whether the lesion was proximal or distal to the dorsal root ganglion. The pain had begun spontaneously 2 weeks previously and slowly increased over several hours. Because of pain, testing motor strength in the right lower extremity was very difficult. The saphenous sensory response is absent on the right side and normal on the left. The abnormal saphenous sensory potential on the right corresponds to the abnormal area of sensation on the neurologic examination and also indicates that there has been enough time for wallerian degeneration to have occurred. The abnormalities in the thigh adductors clearly indicate that the lesion is beyond the distribution of the femoral nerve. The remainder of the needle examination, including the right medial gastrocnemius, tibialis anterior, extensor hallucis longus, and L3­L5 paraspinal muscles, are normal. To summarize, abnormalities are found in the distribution of the femoral (vastus lateralis, iliacus) and obturator (thigh adductors) nerves but not in the paraspinal muscles. How Does One Determine the Time Course of the Lesion by these Electrodiagnostic Studies The history of acute onset of groin pain in a hemophiliac, with an absent knee jerk and hypesthesia in the distribution of the saphenous nerve, suggests a retroperitoneal hemorrhage with subsequent compression of the lumbar plexus. The electrodiagnostic studies are consistent with a lesion of the lumbar plexus, most likely caused by compression secondary to a hematoma. Chapter 35 · Lumbosacral Plexopathy 637 she developed severe, boring toothache-like pain in the right hip and thigh that radiated down her leg.

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This pattern often is mistaken for axonal loss and probable polyneuropathy by many electromyographers pulse pressure of 96 order terazosin in united states online. The key to not mistaking this pattern for a polyneuropathy with axonal loss is first recognizing that the sensory potentials are normal pulse pressure amplification cheap terazosin 5 mg without prescription. Few axonal polyneuropathies have normal sensory potentials with reduced motor responses blood pressure 700 cheap terazosin 5 mg with mastercard. On reviewing the history further blood pressure khan academy cheap terazosin online visa, the patient reported a 40-pack-per-year history of smoking blood pressure medication ed generic terazosin 2 mg free shipping. Could the Original Diagnoses of Motor Neuron Disease and Guillain-Barré Syndrome Have Been Correct One can appreciate that the proper electrophysiologic study dramatically changed the evaluation and subsequent therapy of this patient. The original diagnoses of motor neuron disease and Guillain-Barré syndrome were inaccurate. However, the subsequent nerve conduction studies did not substantiate any type of demyelinating neuropathy. Within a few hours, she rapidly developed diplopia and dysarthria, followed quickly by bifacial weakness, ptosis, and respiratory compromise. There was marked bifacial weakness, ptosis, dysarthria, and dysphagia and weakness of proximal greater than distal muscles. The remainder of the neurologic examination, including mental status and sensation, were normal. There was no history of toxin exposure, recent travel, tick bite, viral illness, or vaccinations. Laboratory studies showed unremarkable blood chemistries and normal cerebrospinal fluid examination. Subsequently, the patient revealed that she had tasted some home-preserved peaches but had discarded the canning jar because it smelled rancid. Trivalent botulinum antitoxin was administered within 24 hours, with slight clinical improvement over the next week. Clostridium toxin type B was isolated in the stool extract and from the residue from the canning jar, but it was not found in the serum. Summary the history is that of a woman presenting with the acute onset of rapidly progressive bulbofacial, extraocular, respiratory, and proximal limb muscle weakness, accompanied by poor pupillary responses and areflexia. There is no history of toxin exposure, recent travel, tick bite, flu, or vaccinations. How Do the Electrodiagnostic Findings in Botulism Relate to the Underlying Pathophysiology The unique electrophysiologic findings in botulism reflect the underlying pathophysiology of botulinum poisoning. Electrodiagnostic testing helps differentiate botulism from other paralytic disorders, including Guillain-Barré syndrome, tick paralysis, poliomyelitis, porphyria, and organophosphate poisoning. Furthermore, demyelinating forms of Guillain-Barré syndrome usually reveal acquired demyelination on nerve conduction studies. Acute poliomyelitis generally presents as a febrile illness followed within days by focal, asymmetric paralysis. Organophosphate poisoning may present with acute weakness, but miosis and fasciculations differentiate this poisoning from botulism. Ten-second exercise is superior to 30-second exercise for post-exercise facilitation in diagnosing Lambert­Eaton myasthenic syndrome. As noted earlier, Guillain-Barré syndrome is among the disorders that can result in rapidly progressive paralysis. The Lambert­ Eaton myasthenic syndrome: a cause of delayed recovery from general anesthesia. Myasthenic syndrome due to defects in rapsyn: clinical and molecular findings in 39 patients. Reference values for jitter recorded by concentric needle electrodes in healthy controls: a multicenter study. It is always desirable to biopsy an unequivocally abnormal muscle yet one that is not end stage. In addition, neuromuscular ultrasound can add key information in selected cases of myopathy, and is discussed later in the chapter. In most myopathies, symptoms tend to be bilateral and affect proximal muscles preferentially. Patients usually complain of difficulty rising from chairs, going up and down stairs, or reaching with their arms. Although most myopathies are symmetric and proximal, there are exceptions to both. Deep tendon reflexes are generally preserved or, if reduced, are in proportion to the degree of muscle wasting and weakness. In evaluating a patient with suspected myopathy, it is important to determine whether symptoms are exercise induced. Such symptoms may manifest as fatigability, exerciseinduced muscle cramps, or swelling. Patients who present with exercise-induced muscle cramps (see later) may develop frank weakness, swelling, and, if severe enough, myoglobulinuria. In addition, adult onset spinal muscular atrophy, including X-linked bulbospinal muscular atrophy, usually presents with proximal muscle weakness and mimics the typical pattern of a myopathy. Muscular dystrophies are inherited muscle disorders characterized by a progressive course and often an early onset, usually with a specific clinical and muscle biopsy pattern. The more common muscular dystrophies include myotonic dystrophy, Duchenne muscular dystrophy, Becker muscular dystrophy, Emery-Dreifuss muscular dystrophy, facioscapulohumeral muscular dystrophy, oculopharyngeal muscular dystrophy, and the limb girdle muscular dystrophies. Other types of inflammatory myopathy include those caused by muscle infection by parasites, viruses, or bacteria. These agents inhibit normal physiologic mechanisms that protect against autoimmunity. However, on muscle biopsy, there are many necrotic fibers with little or no inflammation. Risk factors include statin use wherein patients develop an autoimmune response to statins, malignancy, and connective tissue diseases. Endocrine myopathies are often seen in disorders of the thyroid and adrenal glands. In addition, myopathy can accompany some cases of acromegaly and parathyroid disease. Examples of common drug-induced and toxic myopathies include those caused by steroids, alcohol, colchicine, azidothymidine, clofibrate, and as a direct toxic effect of many of the cholesterol-lowering agents. Chapter 38 · Myopathy 677 Metabolic myopathies are disorders of muscle resulting from inherited enzyme deficiencies important in intracellular energy production. They may present in one of three ways: (1) as cramps and myoglobinuria, (2) as part of a more diffuse neurologic syndrome, often involving the central nervous system, or (3) as a typical clinical proximal myopathy. In patients with cramps and myoglobinuria, the genetic defect often is found either in the glycogen or lipid metabolism pathways. These patients may be completely normal at rest but become symptomatic during or after exercise. In patients with disorders along the lipid pathway, symptoms commonly occur after an episode of long or forced exercise. In patients with disorders along the glycogen pathway, symptoms commonly occur after brief, intense isometric exercise. Muscle aches and fatigue may begin during the exercise, followed by frank myoglobinuria. Patients with defects in mitochondrial metabolism often present with a myopathy, as well as abnormalities involving other systems, including the central nervous system. Short stature, hearing loss, seizures, cardiac abnormalities, learning disabilities, and stroke-like episodes are common. Congenital myopathies are a group of myopathies in which each disorder has a fairly specific muscle biopsy finding on histochemical staining. Although most patients present in the first few years of life, an occasional patient with a congenital myopathy presents in adulthood with one of these disorders. The clinical syndromes are nonspecific and tend to be slowly progressive or static. Genetic testing or muscle biopsy usually is needed for definitive diagnosis, unless there is a known confirmed diagnosis in the family. Myopathy associated with periodic paralysis occurs in the setting of hypokalemic and hyperkalemic periodic paralysis (see Chapter 39). Even those patients with hypokalemic periodic paralysis who have never experienced episodic weakness, a common scenario in affected females, invariably will develop a proximal vacuolar myopathy in adulthood. At least one motor and one sensory conduction study and corresponding F responses from the upper extremity. At least one motor and one sensory conduction study and corresponding F responses from the lower extremity. If a significant decrement is found with 3-Hz repetitive nerve stimulation of any muscle, then proceed with further testing, looking for a disorder of the neuromuscular junction (see Chapter 37, Box 37. Rarely, neuromuscular junction disorders will present with proximal weakness, normal nerve conduction studies, and "myopathic" motor unit action potentials on needle electromyography. Sensory nerve conduction studies are always normal, unless there is a coexistent neuropathy. Because most myopathies preferentially affect proximal muscles and routine motor nerve conduction studies record distal muscles, motor nerve conduction studies are also usually normal. The major reason nerve conduction studies must be performed is to exclude other motor disorders that may mimic myopathy (Box 38. The nerve conduction studies in motor neuron disease and myopathies that affect distal muscles may be very similar. Nerve conduction studies can easily differentiate demyelinating polyneuropathy from myopathy by the presence of conduction block or temporal dispersion, marked slowing of distal latencies and conduction velocity, or a combination of these findings. At least one paraspinal muscle Special considerations: lwaystrytostudyweakmuscles. Thenumberand · A distribution of muscles studied depend on the pattern of weakness. Calculate the mean amplitude and duration and compare with agematched controls for the muscle sampled. Repetitive nerve stimulation should be performed first; if normal, singlefiber electromyography should be considered. Overall, examining distal and proximal muscles in both the upper and lower extremities is indicated. As most myopathies affect proximal muscles, the yield of finding abnormalities increases as progressively more proximal muscles are sampled. In adult-onset acid maltase deficiency myopathy, for instance, prominent changes may be seen only in the most proximal muscles (paraspinals, diaphragm, and tensor fascia latae). This is most commonly seen in steroid myopathy and some metabolic and mitochondrial myopathies. The last issue is that of which muscle to biopsy, because patients with suspected myopathy often go on to muscle biopsy. Spontaneous Activity in Myopathies Fibrillation potentials and positive sharp waves usually are associated with neuropathic disorders. Infarction of small intramuscular nerve twigs by surrounding interstitial inflammation also is speculated to be a possible cause Chapter 38 · Myopathy 679 Box 38. Although the presence of denervating potentials in a patient with myopathy often suggests the diagnosis of an inflammatory myopathy, denervating potentials can occur in a variety of myopathies (Box 38. A myotonic discharge is the spontaneous firing of a muscle fiber that waxes and wanes in both amplitude and frequency. The morphology of a myotonic discharge is either a positive wave or a brief spike potential. This should not be surprising because myotonic discharges are generated by muscle fibers as well. Myotonic discharges can be differentiated from fibrillation potentials and positive sharp waves by the waxing and waning of both firing frequency and amplitude. Remember that fibrillation potentials and positive sharp waves, in contrast, fire at a very regular rate. Myotonic discharges may be seen in myotonic dystrophy (types 1 and 2), myotonia congenita, paramyotonia congenita, and hyperkalemic periodic paralysis. They can also be seen in other myopathies, including acid maltase deficiency (especially in the paraspinal muscles), myotubular (centronuclear) myopathy, some drug-induced myopathies. Superficially, a muscle cramp and a contracture may appear similar clinically-the painful involuntary contraction of a muscle. Only in the rare case of a very severe myopathy where every muscle fiber in a motor unit drops out does the effective number of motor units decrease. In myopathy, motor unit territory typically decreases in size as individual muscle fibers drop out. Sometimes muscle fibers from the same motor unit are in close contact, either from muscle fiber splitting or after reinnervation in those myopathies associated with denervating features. Duration most closely reflects the total number of muscle fibers in a motor unit, including those muscle fibers at a distance from the recording electrode. Any disorder that effectively causes loss or dysfunction of individual muscle fibers. A similar situation occurs in early reinnervation after severe denervation, when only a few fibers have successfully reinnervated, resulting in nascent (early reinnervated) motor unit potentials, which are also short and small. These findings likely are secondary to fiber splitting or collateral sprouting from reinnervation in those myopathies associated with necrosis and subsequent denervation. In myopathy, the amplitude commonly is decreased, but it can also be normal or increased if the needle electrode is placed near split or reinnervated fibers. The number of phases is primarily a measure of synchrony, and polyphasia may be seen in both myopathic and neuropathic disorders. Presumably, many of the remaining muscle fibers are dysfunctional and do not fire as synchronously as normal.

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