Neurology. Charles H. Clarke

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digitorum profundus I, II Median Tip of ring & Vth finger flexion C8 Flexor digitorum profundus IV, V Ulnar Thumb abduction T1 Abductor pollicis brevis Median Finger abduction T1 Dorsal interossei Ulnar Finger flexion (C7), C8, (T1) Long and short flexors Median and ulnar Hip flexion L1, L2, (L3) Iliopsoas Nerve to iliopsoas Hip adduction L2, L3, L4 Adductor magnus Obturator Knee extension L3, L4 Quadriceps femoris Femoral Ankle dorsiflexion L4, L5 Tibialis anterior Deep peroneal Big toe extension L5, (S1) Extensor hallucis longus Deep peroneal Ankle eversion L5, S1 Peroneal muscles Superficial peroneal Ankle inversion L4, L5 Tibialis posterior Tibial Ankle plantar flexion S1, S2 Gastrocnemius, soleus Posterior tibial Knee flexion S1, (S2) Hamstrings Sciatic Hip extension S1, (S2) Gluteus maximus Inferior gluteal

      Root pain caused by distortion or stretching of meninges surrounding a root is perceived both in the myotome and the dermatome. This is relevant in C7 root compression: pain can be felt deep to the scapula (C7 muscles) while the sensory disturbance runs to the middle finger (C7 dermatome). The triceps jerk is lost. See Chapters 10 and 16.

      Cauda Equina Syndrome

      A lesion of the conus medullaris, the lowermost cord, such as an MS plaque can cause difficulty. Weakness, sensory loss and loss of sphincter control also occur, and with an acute conus lesion tendon reflexes can also be lost, as with the cauda equina. Extensor plantars and sensory loss typical of a cord lesion, such as a sensory level or Brown‐Séquard signs should enable distinction clinically, before imaging.

      Myopathy

      Muscle disease tends to produce symmetrical abnormalities (Chapter 10).

      Inflammatory disease, such as polymyositis, causes induration, pain and weakness. Dystrophies and most metabolic muscle diseases present typically with weakness alone; pseudohypertrophy (excessively bulky muscles) may develop. Slow relaxation is a feature of myotonic conditions. Fatiguability is characteristic of myasthenia gravis, and the reverse, an increase in power on exercise is sometimes seen in LEMS.

      Subacute Paralysis

      This describes increasing limb weakness, up to an arbitrary 3 weeks. Cord compression, poliomyelitis, Guillain–Barré, other neuropathies, MS, myasthenia, LEMS, botulism are potential causes (Chapters 9, 10, and 11). Respiratory impairment is easy to miss with limb weakness. Initial paralytic symptoms are regarded as non‐organic in about one‐quarter when patients first seek help.

      Symptoms that are unexplained or only partially explained by organic disease are common. Deliberate exaggeration and even fabrication were thought to be more frequent than current views suggest, perhaps now erring towards political correctness. The reality is that many have symptoms that are worrying or uncomfortable but do not reflect any serious disease – for example, unexplained fatigue, give‐way weakness and non‐organic sensory loss, or ‘attacks’. The problem is serious: about one‐third of apparent status epilepticus and a fifth of recurrent attacks referred to epilepsy clinics are non‐organic (see also Chapter 22).

      One approach is to accept that the majority do have the symptoms of which they complain. This comment excludes those involved in legal claims, where non‐organic features are especially prominent and of a more doubtful nature. The second suggestion is to exclude organic disease with all reasonable certainty. A third is to understand the psychiatric diagnoses, such as depression that might explain such symptoms. Abnormal illness behaviour or somatoform disorder (now known as Somatic Symptom Disorder in DSM‐5) are other potential explanations. However, in many cases of apparent illness behaviour, no formal psychiatric diagnosis is apparent.

      I am most grateful to Matthew Adams, Robin Howard, Martin Rossor, Simon Shorvon & Jason Warren for their help with our chapter in Neurology A Queen Square Textbook Second Edition, upon which this text is based.

      The late Dr Anthony Hopkins (1937–1997) my consultant colleague at St Bartholomew’s Hospital in the 1980s and 1990s provided me with inspiration – and also talked much common sense.

      1 Clarke

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