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The Peripheral Neuropathy Solution

Dr. Labrum Peripheral Neuropathy Solution

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Introduction 1

Tools 5

Cranial nerves 31

Olfactory nerve 33

Optic nerve 35

Oculomotor nerve 39

Trochlear nerve 43

Trigeminal nerve 46

Abducens nerve 53

Facial nerve 56

Acoustic nerve 62

Vestibular nerve 64

Glossopharyngeal nerve 67

Vagus nerve 70

Accessory nerve 74

Hypoglossal nerve 77

Cranial nerves and painful conditions - a checklist 80

Cranial nerve examination in coma 81

Pupil 82

Multiple and combined oculomotor nerve palsies 84

Plexopathies 87

Cervical plexus and cervical spinal nerves 89

Brachial plexus 91

Thoracic outlet syndromes (TOS) 104

Lumbosacral plexus 106

Radiculopathies 117

Cervical radiculopathy 119

Thoracic radiculopathy 126

Lumbar and sacral radiculopathy 129

Cauda equina 137

Mononeuropathies 141

Introduction 143

Mononeuropathies: upper extremities 145

Axillary nerve 147

Musculocutaneous nerve 151

Median nerve 154

Ulnar nerve 162

Radial nerve 168

Digital nerves of the hand 173

Mononeuropathies: trunk 175

Phrenic nerve 177

Dorsal scapular nerve 180

Suprascapular nerve 182

Subscapular nerve 184

Long thoracic nerve 186

Thoracodorsal nerve 189

Pectoral nerve 191

Thoracic spinal nerves 192

Intercostal nerves 194

Intercostobrachial nerve 196

Iliohypogastric nerve 197

Ilioinguinal nerve 199

Genitofemoral nerve 201

Superior and inferior gluteal nerves 202

Pudendal nerve 204

Mononeuropathies: lower extremities 209

Obturator nerve 211

Femoral nerve 213

Saphenous nerve 217

Cutaneous femoris lateral nerve 219

Cutaneous femoris posterior nerve 221

Sciatic nerve 222

Peroneal nerve 226

Tibial nerve 230

Tarsal tunnel syndrome (posterior and anterior) 233

Anterior tarsal tunnel syndrome 236

Sural nerve 237

Mononeuropathy: interdigital neuroma and neuritis 239

Nerves of the foot 241

Peripheral nerve tumors 243

Polyneuropathies 247

Introduction 249

Metabolic diseases 253

Diabetic distal symmetric polyneuropathy 253

Diabetic autonomic neuropathy 256

Diabetic mononeuritis multiplex and diabetic polyradiculopathy

(amyotrophy) 258

Distal symmetric polyneuropathy of renal disease 260

Systemic disease

Vasculitic neuropathy, systemic 262

Vasculitic neuropathy, non-systemic 265

Neuropathies associated with paraproteinemias 266

Amyloidosis (primary) 269

Neoplastic neuropathy 271

Paraneoplastic neuropathy 273

Motor neuropathy or motor neuron disease syndrome 276

Infectious neuropathies

Human immunodeficiency virus-1 neuropathy 278

Herpes neuropathy 281

Hepatitis B neuropathy 282

Bacterial and parasitic neuropathies 284

Inflammatory

Acute motor axonal neuropathy (AMAN) 288

Acute motor and sensory axonal neuropathy (AMSAN) 289

Acute inflammatory demyelinating polyneuropathy (AIDP, Guillain-

Barre syndrome) 290

Chronic inflammatory demyelinating polyneuropathy (CIDP) 292

Demyelinating neuropathy associated with anti-MAG antibodies . . . . 295

Miller-Fisher syndrome (MFS) 296

Nutritional

Cobalamin neuropathy 297

Post-gastroplasty neuropathy 299

Pyridoxine neuropathy 300

Strachan's syndrome 301

Thiamine neuropathy 302

Tocopherol neuropathy 303

Industrial agents

Acrylamide neuropathy 304

Carbon disulfide neuropathy 305

Hexacarbon neuropathy 306

Organophosphate neuropathy 307

Drugs

Alcohol polyneuropathy 308

Amiodarone neuropathy 310

Chloramphenicol neuropathy 311

Colchicine neuropathy 312

Dapsone neuropathy 313

Disulfiram neuropathy 314

Polyneuropathy and chemotherapy 315

Vinca alkaloids 316

Platinum-compounds (cisplatin, carboplatin, oxaliplatin) 317

Taxol 318

Metals

Arsenic neuropathy 320

Mercury neuropathy 322

Thallium neuropathy 323

Hereditary neuropathies

Hereditary motor and sensory neuropathy type 1 (Charcot-Marie-Tooth disease type 1, CMT) 324

Hereditary motor and sensory neuropathy type 2 (Charcot-Marie-Tooth disease type 2, CMT) 327

Hereditary neuropathy with liability to pressure palsies (HNPP) 329

Porphyria 331

Other rare hereditary neuropathies 333

Neuromuscular transmission disorders and other conditions 335

Myasthenia gravis 337

Drug-induced myasthenic syndromes 346

LEMS (Lambert Eaton myasthenic syndrome) 349

Botulism 352

Tetanus 354

Muscle and myotonic diseases 357

Introduction 359

Polymyositis 362

Dermatomyositis 365

Inclusion body myositis (IBM) 368

Focal myositis 370

Connective tissue diseases 372

Infections of muscle 375

Duchenne muscular dystrophy (DMD) 380

Becker muscular dystrophy 383

Myotonic dystrophy 385

Limb girdle muscular dystrophy 388

Oculopharyngeal muscular dystrophy (OPMD) 393

Fascioscapulohumeral muscular dystrophy (FSHMD) 396

Distal myopathy 400

Congenital myopathies 403

Mitochondrial myopathies 409

Glycogen storage diseases 413

Defects of fatty acid metabolism 417

Toxic myopathies 420

Critical illness myopathy 423

Myopathies associated with endocrine/metabolic disorders and carcinoma 425

Myotonia congenita 428

Paramyotonia congenita 431

Hyperkalemic periodic paralysis 433

Hypokalemic periodic paralysis 436

Motor neuron disease 439

Amyotrophic lateral sclerosis 441

Spinal muscular atrophies 444

Poliomyelitis 447

Bulbospinal muscular atrophy (Kennedy's syndrome) 451

General disease finder 453

Subject index 469

Introduction

The authors of this book are American and European neurologists. This book is termed a "neuromuscular atlas" and is designed to help in the diagnosis of neuromuscular diseases at all levels of the peripheral nervous system. This book is written for students, residents, physicians and neurologists who do not specialize in neuromuscular diseases.

The first chapter describes the numerous tools used in the diagnosis of neuromuscular disease. These include history taking, the physical examination, laboratory values, electrophysiology, biopsy and genetics. It should help the reader gain an overview of the commonly used methods.

The clinical chapters start with cranial nerves, followed by radiculopathies, plexopathies, mononeuropathies of upper extremities, trunk, lower extremities and polyneuropathies. This is followed by disorders of neuromuscular transmission, muscle and myotonic diseases and motor neuron disease.

The final chapter is called a general disease finder, which helps to identify neuromuscular symptoms and signs associated with general disease.

Each section has a "tool" bar, giving an outline of which examination techniques are most useful. This is followed by anatomical localization, symptoms and signs. The different etiologies are described and are followed by a description of useful diagnostic tests, differential diagnosis, therapy and prognosis. This structured approach occurs through the whole book and allows the reader to follow the same pattern in all sections. A few key references are provided.

Figures and clinical pictures are an essential part of the book. The figures are simple and focus on the essential features of the peripheral structures. We were fortunate to work with artist Jeanette Schulz who put our anatomical requests into clear and distinct figures.

The pictures are of two categories: histological pictures and pictures of patients and diseases. The histologicical pictures were mostly provided by Dr. James Russel who also received neuropathological help from Dr. Mila Blaivas. The clinical pictures were mostly taken by Drs. Grisold and Zifko and reflect a large series of photographic clinical documentation, that was accumulated over the years.

We are aware that for many entities like polyneuropathies, myopathies, and mononeuropathies several excellent monographs and teaching books have been written. However we found no other book which provides a complete overview in a structured and easily comprehensive pattern supported by figures and pictures.

While writing for this book the authors have had fruitful discussions about several disease entities with individuals from the different schools of diagnosis, treatment and teaching in the US and in Europe. We hope that this book will be of clinical help for all physicians working with patients with neuromuscular disease.

Tools

Several important diagnostic tools are necessary for the proper evaluation of a patient with a suspected neuromuscular disorder. Each individual chapter in this book is headed by a "tool bar", indicating the usefulness of various diagnostic tests for the particular condition discussed in the chapter. For example, genetic testing is necessary for the diagnosis of hereditary neuropathy and hereditary myopathy, while nerve conduction velocity (NCV) and electromyography (EMG) can be important but are less specific for these diseases. Conversely, NCV and EMG are the predominate diagnostic tools for a local entrapment neuropathy like carpal tunnel syndrome. Some conditions will require autonomic testing or laboratory tests.

The evaluation of a patient with neuromuscular disease includes a thorough history of the symptoms, duration of the present illness, past medical history, social history, family history, and details about the patient's occupation, behaviors, and habits. Much can be learned from the distribution of the symptoms and their temporal development. The types of symptoms (motor, sensory, autonomic, and pain) need to be addressed in detail.

The history is followed by a clinical examination, which will assess signs of muscle weakness, reflex and sensory abnormalities, and autonomic changes, as well as give information about pain and impairment. The clinical examination is of utmost importance for several reasons. The findings will correlate with the patient's symptoms, and the distribution of the signs (e.g. muscle atrophy in muscle disease) may be a significant diagnostic clue. Documentation of the course of signs and symptoms will be useful in monitoring disease progression, and may guide therapeutic decisions.

Documentation of the progression of neuromuscular disease (especially chronic diseases) should not be limited to changes measured by the ancillary tests described later in this section. Depending upon the disease, measurement of muscle strength, sensory measurements (e.g., vibration threshold, Semmes-Weinstein filaments, etc.), and sketches of the patterns of atrophy and weakness may be helpful. Digital imaging, video clips, and photographs of patients provide a precise documentation of the patient's movement capabilities, but may not be possible due to legal, ethical, and other concerns for the patient.

The diagnostic hypothesis developed by the history and clinical exam can be confirmed by ancillary testing. Ancillary tests can also be used to monitor the stabilization or progression of the disease, and the impact of therapies. Standard electrophysiological tests include NCV, EMG, and repetitive nerve stimulation. Laboratory tests, such as creatine kinase, electrolyte assessment, and antibody testing (e.g. myasthenia gravis, MG) may also be necessary. Genetic testing has become an important tool in the last twenty years, and can be used in many diseases to confirm a precise diagnosis. Some other tests, like autonomic testing (such as the Ewing battery and others) and quantitative sensory testing may not be available in some areas. Finally, neuroimaging can also provide information. MRI can be used to assess muscle inflammation and atrophy, and compression or swelling of peripheral nerves.

The following description of diagnostic tools is intended to be a brief overview, with references for further reading.

The patient with neuromuscular disease

Fig. 1. Anatomy of peripheral nerve. A peripheral nerve consists of bundles of axons surrounded by and embedded in a collagen matrix. The outer connective tissue covering is called the epineurium. The inner connective tissue that divides the axons into bundles is called the perineurium. The innermost layer of connective tissue surrounding the individual axons is called the endoneurium. Blood vessels and connective tissue cells such as macrophages, fibroblasts and mast cells are also contained within the peripheral nerve. The arrow (a) indicates an enlarged view of an individual axon and its surrounding Schwann cells. A node of Ranvier, the space between adjacent Schwann cells is depicted as the narrowing of the sheath surrounding the axon. Each internode is formed by a single Schwann cell

Fig. 1. Anatomy of peripheral nerve. A peripheral nerve consists of bundles of axons surrounded by and embedded in a collagen matrix. The outer connective tissue covering is called the epineurium. The inner connective tissue that divides the axons into bundles is called the perineurium. The innermost layer of connective tissue surrounding the individual axons is called the endoneurium. Blood vessels and connective tissue cells such as macrophages, fibroblasts and mast cells are also contained within the peripheral nerve. The arrow (a) indicates an enlarged view of an individual axon and its surrounding Schwann cells. A node of Ranvier, the space between adjacent Schwann cells is depicted as the narrowing of the sheath surrounding the axon. Each internode is formed by a single Schwann cell

Axono Cachexia

Fig. 2. Below: The axon (a) is surrounded by layers of Schwann cell cytoplasm and membranes. The Schwann cell cytoplasm is squeezed into the outer portion of the Schwann cell leaving the plasma-lemmae of the Schwann cell in close apposition. These layers of Schwann cell membrane contain specialized proteins and lipids and are known as the myelin sheath. Above: Peripheral axons are surrounded by as series of Schwann cells. The space between adjacent Schwann cells are called Nodes of Ranvier (*). The nodes contain no myelin but are covered by the outer layers of the Schwann cell cytoplasm. The area covered by the Schwann cell is known as the internode

Fig. 2. Below: The axon (a) is surrounded by layers of Schwann cell cytoplasm and membranes. The Schwann cell cytoplasm is squeezed into the outer portion of the Schwann cell leaving the plasma-lemmae of the Schwann cell in close apposition. These layers of Schwann cell membrane contain specialized proteins and lipids and are known as the myelin sheath. Above: Peripheral axons are surrounded by as series of Schwann cells. The space between adjacent Schwann cells are called Nodes of Ranvier (*). The nodes contain no myelin but are covered by the outer layers of the Schwann cell cytoplasm. The area covered by the Schwann cell is known as the internode

Fig. 3. Sensory information is relayed from the periphery towards the central nervous system through special sensory neurons. These are pseudo-unipolar neurons located within the dorsal root ganglia along the spinal cord. Mechanical, temperature and noxious stimuli are transduced by special receptors in the skin into action potentials that are transmitted to the sensory neuron. This neuron then relays the impulse to the dorsal horn of the spinal cord

General examination

Neuromuscular clinical phenomenology

Motor function

As already pointed out above, the case history is the basis of the clinical examination. Before assessing the patient in detail, the general examination may give clues to underlying disease (e.g., diabetes, thyroid disease, toxic or nutritional problems). The family history may suggest genetic diseases. Changes of the skeletal system (e.g., kyphosis, scoliosis, atrophy, hypertrophy, and abnormal muscle movements) may indicate neuromuscular disease. Skin changes to watch for include signs of vasculitis, cafe-au-lait spots, patchy changes from leprosy or radiation, and the characteristic changes associated with dermatomyositis.

Motor dysfunction is one of the most prominent features of neuromuscular disease. The patient's symptoms may include weakness, fatigue, muscle cramps, atrophy, and abnormal muscle movements like fasciculations or myo-kymia. Weakness often results in disability, depending on the muscle groups involved. Depending on the onset and progression, weakness may be acute and debilitating, or may remain discrete for a long time. As a rule, lower extremity weakness is noticed earlier due to difficulties in climbing stairs or walking. The distribution of weakness is characteristic for some diseases, and proximal and distal weakness are generally associated with different etiologies. Fluctuation of muscle weakness is often a sign of neuromuscular junction disorders.

Weakness and atrophy have to be assessed more precisely in mononeurop-athies, because the site of the lesion can be pinpointed by mapping the locations of functional and non-functional nerve twigs leaving the main nerve trunk.

Muscle strength can be evaluated clinically by manual and functional testing. Typically, the British Medical Research Council (BMRC) scale is used. This simple grading gives a good general impression, but is inaccurate between grades 3 and 5 (3 = sufficient force to hold against gravity, 5 = maximal muscle force). A modified version of the scale has subdivisions between grades 3 and 5. A composite BMRC scale can be used for longitudinal assessment of disease. Quantitative assessment of muscle power is more difficult because a group of muscles is usually involved in the disease, and cannot really be assessed accurately. Handgrip strength can be measured by a myometer, and can be useful in patients with generalized muscle weakness involving the upper extremities.

Fatigability is present in many neuromuscular disorders. It can be objectively noted in neuromuscular transmission disorders like myasthenia gravis (e.g., ptosis), and is also present in neuromuscular diseases like amyotrophic lateral sclerosis (ALS), muscular dystrophies, and metabolic myopathies, where it appears to be caused by activity.

Muscle wasting can be generalized or focal, and may be difficult to assess in infants and obese patients. Asymmetric weakness is usually noted earlier, in particular, the intrinsic muscles of the hand and foot. Muscle wasting may also occur in immobilization (either due to medical conditions like fractures, or persistent immobility from rheumatoid diseases with joint impairment) and in wasting due to malnutrition or cachexia caused by malignant disease.

Muscle hypertrophy is much rarer than atrophy and may be generalized, as in myotonia congenita, or localized, as in the "pseudohypertrophy" of the calf muscles in some types of muscular dystrophy and glycogen storage diseases. Focal hypertrophy is even rarer and may occur in muscle tumors, focal myositis, amyloidosis, or infection. Also, ruptured muscles may mimic a local hypertrophy during contraction.

Abnormal muscle movements can be the hallmark of a neuromuscular condi- Abnormal muscle tion and should be observed at rest, during and after contraction, and after movements percussion.

- Fasciculations are brief asynchronous twitches of muscle fibers usually apparent at rest. They may occur in healthy individuals after exercise, or after caffeine or other stimulant intake. Cholinesterase inhibitors or theophylline can provoke fasciculations. Fasciculations are often associated with motor neuron disease [ALS, spinal muscular atrophy (SMA)], but can also occur in polyneuropathies, and be localized in radiculopathies. Contraction fasciculations appear during muscle contraction, and are less frequent.

- Myokymia is defined as involuntary, repeated, worm-like contractions that can be clearly seen under the skin ("a bag of worms"). EMG shows abundant activity of single or grouped, normal-appearing muscle unit potentials, and is different from fasciculations. Myokymia is rare and appears in neuromuscular disease with "continuous muscle fiber activity", such as Isaac's syndrome, and in CNS disease (e.g. brainstem glioma). Myokymia may be a sequel of radiation injury to the peripheral nerves, most frequently seen in radiation plexopathies of the brachial plexus.

- Neuromyotonia, or continuous muscle fiber activity (CMFA), is rare. It results in muscle stiffness and a myotonic appearance of movements after contraction. Rarely, bulbar muscles can be involved, resulting in a changed speech pattern. The condition can be idiopathic, appear on a toxic basis (e.g., gold therapy) or on an autoimmune basis.

- Myoedema occurs after percussion of a muscle and results in a ridge-like mounding of a muscle portion, lasting 1-3 seconds. It is a rare finding and can be seen in hypothyroidism, cachexia, or rippling muscle disease.

- Rippling muscle is a self-propagating rolling or rippling of muscle that can be elicited by passive muscle stretch. It is an extremely rare phenomenon. Percussion can induce mounding of the muscle (mimicking myoedema). The rippling muscle movement is associated with electrical silence during EMG.

- Myotonia occurs when a muscle is unable to relax after voluntary contraction, and is caused by repetitive depolarizations of the muscle membrane. Myotonia is well characterized by EMG. It occurs in myotonic dystrophies and myotonias.

- Action myotonia is most commonly observed. The patient is unable to relax the muscles after a voluntary action (e.g. handgrip). This phenomenon can last up to one minute, but is usually shorter (10-15 seconds). Action myotonia diminishes after repeated exercise (warm up phenomenon), but may conversely worsen in paramyotonia congenita.

- Percussion myotonia can be seen in all affected muscles, but most often the thenar eminence, forearm extensors, tibialis anterior muscle or the tongue are examined. The relaxation is delayed and a local dimple caused by the percussion appears, lasting about 10 seconds.

- Pseudoathetosis is a characteristic of deafferentiation and loss of position sense. Fine motor tasks are impaired or markedly slowed, and result in a writhing and undulating movement pattern of outstretched fingers, aggravated with eye closure. Pseudoathetosis appears in sensory neuropathies, posterior column degeneration, and tabes dorsalis.

- Moving toes: Length dependent distal neuropathies may be associated with moving toes. This sign may be due to large sensory fiber loss, and has been observed in cisplatinum induced neuropathies.

- Neuropathic tremor resembles orthostatic tremor and has a frequency of 3-6 Hz. It occurs in asscociation with demyelinating neuropathies.

- Muscle cramps are painful involuntary contractions of a part or the whole muscle. At the site of the contraction a palpable mass can be felt. EMG reveals bursts of motor units in an irregular pattern. Cramps often occur in the calves, and can be relieved by stretching. Cramps may occur in metabolic conditions (electrolyte changes), motor neuron disease, some myopathies, and some types of polyneuropathy.

- Stiff person syndrome is characterized by muscle stiffness and spasms due to synchronous activation, predominantly of trunk muscles. EMG reveals normal muscle unit potentials firing continuously. This disease, though producing muscle symptoms, is a central disease due to a disinhibited gaba receptor. It occurs in autoimmune or paraneoplastic disease.

References Aids to the examination of the peripheral nervous system. WB Saunders, London (1986)

Carvalho M de, Lopes A, Scotto M, et al (2001) Reproducibility of neurophysiological and myometric measurement in the ulnar nerve abductor digiti minimi system. Muscle Nerve 24:1391-1395

Hart IK, Maddison P, Newsom-Davies J, et al (2002) Phenotypic variants of autoimmune peripheral nerve hyperexcitability. Brain 125: 1887-1895

Merkies LSJ, Schmitz PIM, Samijn JPA (2000) Assessing grip strength in healthy individuals and patients with immune-mediated polyneuropathies. Muscle Nerve 23: 1393-1401 Suarez GA, Chalk CH, Russel JW, et al (2001) Diagnostic accuracy and certainty from sequential evaluations in peripheral neuropathy. Neurology 57: 1118-1120

Reflex testing The long reflex arch tested by the deep tendon reflex is useful for neuromuscu lar diagnosis, as it reflects both the function of sensory and motor divisions of the local segment tested. It also provides information about the status of the central influence on the local segment being assessed by the quality of the reflex (exaggerated, brisk, normal, diminished). In polyneuropathies the reflexes tend to be diminished or absent, with a tendency towards distal loss in length-dependent neuropathies. A mosaic pattern of reflex activity may point to multifocal neuropathies or multisegmental disorders. Reflexes in myopathies are usually preserved until late stages of the disease (in Duchenne's dystrophy, knee jerks are often absent prior to ankle jerks). Exaggerated and brisk reflexes in combination with weakness and atrophy are suggestive of a combined lesion of lower and upper motor neurons, as in ALS.

Reflexes may be absent at rest and reappear after contraction or repeated tapping ("facilitation") as seen characteristically in the Lambert Eaton syndrome. The reflex pattern pinpoints the site of the lesion, such as with radiculopathies and cervical or lumbar stenosis, where the pattern of elicitable and

Superficial Peroneal Nerve Motor Point
Fig. 4. a 1 Axillary nerve, 2 Superficial radial nerve, 3 Median nerve, 4 Ulnar nerve, 5 Femoral nerve, 6 Sapheneous nerve, 7 Peroneal nerve. b 1 Axillary nerve, 2 Superficial radial nerve, 3 Ulnar nerve, 4 Cutaneous femoris posterior nerve, 5 Sural nerve

absent reflexes (inversion) or combination with long tract signs gives important clues.

Reference Aramideh M, Ongerboer de Visser BW (2002) Brainstem reflexes: electrodiagnostic tech niques, physiology, normative data, and clinical applications. Muscle Nerve 26: 14-30

Muscle tone Muscle tone is an important issue in neuromuscular disease in ALS patients and

"the floppy infant".

Sensory disturbances Sensory disturbances signal disease of the peripheral nerve or dorsal root ganglia and include a spectrum of positive and negative phenomena. The patient is asked to provide a precise description and boundaries of sensory loss (or parasthesias). Reports of permanent, undulating, or ictal (transient) loss or sensations should be noted.

Focal Musculocutaneous Mononeuropathy

A Vibration can be assessed with a Rydel Seiffert tuning fork; B Clinical assessment of position sense; C Vibrometer allows quantitative assessment of vibration threshhold

A Weinstein filaments; B Simple test for temperature discrimination; C Graeulich „star" for two point discrimination a Small fiber, testing by thermal theshhold. The finger is put on a device, which changes temperature. The patient is requested to report changes of temperature or pain. b Vibration threshhold can be assessed electronically and displayed on the screen

Fig. 5. Sensory testing mehtods

Table 1.

Sensory quality

Method*

Fiber type

Light touch Pressure

Brush, examiner's finger tips Semmes Weinstein filaments

All types

Small and large fibers -quantification possible

Pain

Temperature Vibration Position sense

Pin prick

Temperature threshold devices Tuning fork

Small fibers Small fibers Large fibers Large fibers Large fibers

Two point discrimination

Graeulich device

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